The aim of this study was to investigate the impact of left atrial diverticula (LADs), left sided septal pouches (LSSPs) and middle right pulmonary veins (MRPVs) on recurrent atrial fibrillation (rAF) in patients undergoing laser pulmonary vein isolation procedure (PVI).This retrospective study enrolled 139 patients with pre-procedural multiple detector computed tomography (MDCT) imaging and 12 months follow-up examination. LADs, LSSPs and MRPV were identified by two radiologists on a dedicated workstation using multiplanar reconstructions and volume rendering technique. Univariate and bivariate regression analyses with patient demographics and cardiovascular risk factors as covariates were performed to reveal independent factors associated with rAF.LADs were recorded in 41 patients (29%), LSSPs in 20 (14%) and MRPVs in 15 (11%). The right anterosuperior wall of the left atrium was the most prevalent location of LADs (68%). rAF occured in 20 patients, thereof, 15 exhibited an outpouching structure of the left atrium . Presence of an LAD  and permanent AF  were independently associated with rAF.LAD, LSSP and MRPV were common findings on pre-procedural cardiac computed tomography. LADs were revealed as potential independent risk factor of rAF, which might be considered for treatment planning and post-treatment observation. Atrial fibrillation (AF) affects 1% to 2% of the general population, thus representing the most prevalent cardiac arrhythmia . The lifThe aim of this study is to investigate if there is a correlation between LAD, MRPV, LSSP and recurrence of atrial fibrillation (rAF) following pulmonary vein isolation.The Ethics Commission of Cologne University’s Faculty of Medicine approved this retrospective, single-center study (reference number 19–1439). Due to the retrospective nature of the study, a written informed consent was waived.A structured database query of the picture archiving and communication system (PACS) revealed all patients who received a contrast enhanced electrocardiogram-gated multidetector computed tomography of the heart between January 2013 to September 2014 prior to pulmonary vein isolation. All ablations were performed by laser pulmonary vein ablation technique. This resulted in 150 patients screened for study inclusion. Patients with incomplete imaging (N = 6), incomplete ablation procedure with incomplete circumferential lines around the pulmonary veins during catheter ablation (N = 3) or incomplete follow-up visits (N = 5) were excluded from further analysis. In all three cases of incomplete ablation procedure, the anatomy of the esophagus was unfavorable and a complete ablation could not be performed to avoid heat damage.™, GE Healthcare, Waukesha, WI), slice thickness 0.625 mm, section increment 0.1 mm.Cardiac computed tomography was performed using a dedicated scan-protocol with visual triggering of the contrast medium bolus in the left atrium. All studies were carried out using a 64 row MDCT scanner . Scanning was performed in craniocaudal direction from above the aortic arch to the diaphragm using prospective ECG-gating. Using a power injector, 60 ml of an intravenous contrast agent  was administered at a flow rate of 5.0 ml/s through a cubital vein. The contrast bolus was followed by a saline chaser of 50ml at the same flow. No premedication was given. Further scan parameters comprised: 120kV, 200 mAs with tube current modulation. Images were reconstructed using the following parameters: CardIQ Xpress . Two radiologists with 5 and 15 years of experience in cardiac imaging  reviewed the images in consensus using multiplanar reconstructions and volume-rendering techniques. Radiologists were blinded to all clinical data except age and gender. Presence of LAD including the location, LSSP and MRPV were recorded . Left at™, CardioFocus, Marlborough, MA, US). It is a visually controlled laser ablation system consisting of a console, a 15-Charrière outer diameter steerable transseptal sheath, a reusable 2-Charrière endoscope, and the 12-Charrière catheter containing a size-adjustable balloon at the distal end. The console is used to deliver the laser energy, visualize the endoscopic image, and control the balloon size [Pulmonary vein isolation was performed with the “CardioFocus HeartlightTM” system using laser energy  and subsequent fluoroscopic and transesophageal echocardiographically controlled single puncture of the atrial septum using a transeptal needle (BRK) XS 71cm ™, St. Jude Medical, St. Paul, USA). This was followed by a semi-selective angiographic display of all pulmonary veins in left anterior oblique 50° (LAO) and right anterior oblique 25° (RAO) with high-frequency stimulation of the right ventricle (rapid pacing), with a cycle length of between 240 ms and 300 ms. An esophageal temperature probe  was used to measure the esophageal temperature in all patients. To avoid phrenic lesions, the compound motor action potential method (CMAP) was used to isolate the right pulmonary veins. If present, MRPV were targeted by laser balloon. Accessory PVs were not specifically targeted, because they were not present. During the ablation of the right pulmonary veins, the phrenic nerve was stimulated with an electrophysiological diagnostic catheter  in the superior vena cava and the resulting diaphragmatic electromyogram monitored with surface electrodes. After ablation is complete, isolation success is verified using a multipolar circular mapping catheter .All procedures were carried out under anesthesiologic supervision in analgesia with propofol and remifentanil in a cardiac catheter laboratory with a biplane, swiveling X-ray fluoroscopy unit. During the procedure, the patients were heparinized in a controlled manner over the activated clotting time with a target value between 300 and 350 seconds to avoid thromboembolic complications. The measurements were made every 10 to 20 minutes. The left atrial appendage was checked for thrombus using transesophageal echocardiography. Access was via the femoral vein on both sides. A four-pole diagnostic catheter was placed in the right ventricle and a six-pole diagnostic catheter in the coronary sinus after puncturing the left femoral vein and using two 7 F-sheaths. Access to the left atrium was made after puncturing the right femoral vein and placing a long transseptal sheath : age, gender, presence of diabetes mellitus, periphery artery disease, atrial fibrillation, heart failure, hypertension and hyperlipidemia. Additionally, left atrial diameters were given in patients records after transthoracic echocardiogram. The antiarrhythmic drug regimen was as follows: If the patient presented with an existing antiarrhythmic medication  prior to the intervention, it was continued for three additional months after PVI (blanking period). If the patient was not taking any antiarrhythmic medication, no antiarrhythmic medication was started after PVI. Clinical follow-up visits were scheduled 3, 6 and 12 months after ablation and included a holter monitoring for seven days. AF recurrence was defined as the presence of any episode of atrial tachycardia or AF lasting 30 s or more on 12-lead electrocardiogram. Patients with incomplete follow-up visits were excluded from further analysis (n = 5).Categorical variables are presented as numbers with percentages and compared using the Chi-square or the Fisher exact test, when appropriate. Continuous variables are reported as mean ± standard deviation and compared using the two-sided Student’s t-test and the Mann-Whitney-U test, when appropriate. Cut-off values were evaluated with receiver-operating-characteristics curve analysis by determination of the Youden index. Factors with a p-value < 0.2 in the univariate analyses were entered into a binary logistic regression to identify independent factors associated with the respective outcome measure. Statistical significance was defined as p < 0.05. All analyses were performed using dedicated software .The final study cohort consisted of 139 patients that received 139 cardiac ablations due to atrial fibrillation . The most prevalent cardiovascular risk factors were coronary artery disease and arterial hypertension (63% each). The mean LAEDD was 4.4 ± 0.4 cm.A total of 41 (29%) LADs were identified . Multiple LADs in one patient were not found. In 28 of these cases (68%), the LAD was located in the right anterosuperior wall of the left atrium, 7 (18%) in the left inferoposterior wall, and each 2 (5%) in the right inferoanterior, the left anterosuperior and the left inferoanterior wall, respectively .Most of the LAD were located close to the ostia of the pulmonary veins.Accessory pulmonary veins were not found in the present study cohort. MRPVs were found in 15 (11%) cases and LSSPs in 20 (14%).The overall rAF rate was 14% (20/139), including 8 PV reconnections and unclear cause in 12. Of these 20 patients, 13 (65%) had an outpouching of the left atrial anatomy: Nine (45%) had an LAD, 3 (11%) an MRPV and one (5%) an LSSP. In the univariate analysis, the presence of an LAD was by trend associated with rAF . The other two outpouching types were not significantly associated with rAF . Among pThe aim of this study was to investigate the impact of left atrial diverticula, left sided septal pouches and middle right pulmonary veins on recurrent atrial fibrillation after pulmonary vein isolation. First, the results demonstrated that LAD, LSSP and MRPV were common findings in cardiac CT scans with prevalence rates ranging between 11% and 29%. Second, our data suggest that LADs are independently associated with rAF. Third, persistent AF was a further independent risk factor for rAF.LADs represent a common finding in patients with AF with an imaging prevalence of 29% in the current studies, which is within the range of previous studies , 20. LADSince it is known that muscular sleeves from the left atrium can extend into the wall of pulmonary veins, PVI has been successfully used to disconnect the electrical connection between PVs and the left atrium –37. We dTo our knowledge this is the first study to investigate a possible correlation between LSSP and rAF after PVI. LSSP are defined as “kangaroo pouch-like structures”, that occur when the PFO is absent but the septum primum and septum secundum are not completely fused. A recently published study by Holda et al. could demonstrate that there is an association between the presence of LSSP and cryptogenic stroke. LSSP are also described as a trigger for AF . This maThe drawbacks of our study are the retrospective study design and the small study population number. Furthermore, every patient included in our study had a history of AF. A control group of healthy normal rhythmic patients carrying LAD’s without AF would be helpful to better understand clinical implications from our findings. Furthermore, it is important to emphasize that all patients in this study received antiarrhythmic drugs for 12 months after ablation. This interval seems quite long, but does not distort the long-term results, since several studies could proof, that AADs can prevent early atrial arrhythmias within 2 months after catheter ablation, but do not prevent late arrhythmias . AnotherIn conclusion LAD, LSSP and MRPV are common findings during cardiac computed tomography of the heart. The role of LAD in rAF is still controversial, however logistic regression analysis revealed that presence of a LAD and persistent AF as potential independent risk factors for rAF in our study cohort. At this point, further prospective multicenter studies are needed to fully clarify the clinical significance of these structures within the left atrium and recurrence of atrial fibrillation.S1 Data(XLSX)Click here for additional data file.


The main challenges in heart failure (HF) treatment are to manage patients with refractory acute decompensated HF and to stabilize the clinical status of a patient with chronic heart failure. Beyond the use of medications targeted in the inhibition of the neurohormonal system, the balance of salt and fluid plays an important role in the maintenance of clinical compensation in respect of renal function. In the case of heart failure, a debate of opinion exists on salt restriction. Restricted dietary sodium might lead to worse outcomes in heart failure patients due to the activation of the neurohormonal system and malnutrition. On the contrary, positive sodium balance is the primary driver of water retention and, ultimately, volume overload in acute HF. Some recent studies reported associations of decreased salt consumption with higher readmission rates and increased mortality. Thus, the usefulness of salt restriction in heart failure management remains debated. The use of individualized nutritional support, compared with standard hospital food, was effective in reducing these risks, particularly in the group of patients at high nutritional risk. Heart failure (HF) remains one of the leading causes of recurrent hospitalizations, and it poses a large burden on healthcare systems. Even though significant advances in the field of pharmacologic and device therapy have been achieved, it still remains the single most common admission diagnosis in patients aged over 65 years of age . The maiCurrent guidelines recommend restricting sodium intake, ranging from 1500–3000 mg per day, although a debate of opinion still exists regarding the maximum sodium intake for HF patients . High soCongestion has a central role in patients with decompensated heart failure (HF) as it is related to increased morbidity and higher readmission rates, and leads to the vicious cycle of diuretic resistance. The primary mechanism of diuretic resistance in the context of decompensated HF and congestion is increased renal vein pressure, which decreases the arteriovenous pressure gradient, with a parallel increase in the interstitial pressure within the kidney, thereby decreasing renal blood flow, ultrafiltration pressure, and the glomerular filtration rate (GFR). Congestion also exacerbates diuretic resistance by decreasing intestinal absorption and stimulating the SNS and RAAS. Moreover, decreased liver function in patients with right heart failure and congestion leads to hypoalbuminemia, which can increase resistance to furosemide, the most commonly used diuretic. Thus, in a clinical course of patients with decompensated HF, the development of diuretic resistance and progressive cardiorenal dysfunction, despite escalating doses of loop diuretics, resulted in negative outcomes . This isAn important physiological principle of edema formation in acute HF is that a positive sodium balance serves as the primary driver of water retention and, ultimately, volume overload. Although studies have shown that sodium intake leads to the worsening of congestive symptoms, contradictory data have revealed that sodium restriction may not confer a clear benefit with respect to congestive symptoms and clinical outcomes, and it can lead to heightened neurohormonal activity ,8. As anIn the case of pleural effusion, the underlying physiology remains controversial. The fundamental model of pleural exchange in normal conditions involves filtration through the capillaries in the parietal pleura lining the chest wall and drainage of the pleural liquid via lymphatic stomata in the parietal pleura. However, the classical Starling equations do not take into account the electrolyte balance in the formation of the pleural fluid. According to the “chloride theory”, chloride is the key electrolyte for regulating the distribution of body fluid or water in each body compartment ,22,23. UThese findings suggest that, with appropriate patient selection, administration of hypertonic saline to an acute HF patient does not necessarily result in fluid retention or worsening pulmonary edema and hypoxemia. Additionally, an excessive correction of serum sodium should be avoided, and the recommended correction of >6 to 8 mmol/L per 24 h should be maintained in the hyponatremic patient ,26. ReceAnother issue is how to handle fluid overload in HF patients, where the management window between dehydration and overhydration is narrow. The main aim in this situation is to restore fluid balance without risking any further decrease in cardiac performance and stroke volume. In the cases of right heart failure, this balance is difficult to achieve, as low cardiac output in combination with venous congestion and decreased preload leads to progressive renal retention of salt and water. This causes expansion of extracellular space and progressive distention of the myocardium, with adverse effects on cardiac performance. In such cases, the restoration of fluid balance must be cautious to prevent any hemodynamic instability, or it may restore the osmotic gradient within the loop of Henle.In the challenging scenario of acute decompensated HF refractory to all first line treatments with intravenous diuretics and combination of diuretics, ultrafiltration comes to the foreground as a viable solution for fluid removal. It represents a method of energetic withdrawal of isotonic fluid from the venous system, performed with or without the assistance of inotropes and vasospastic drugs. Despite the efficacy of the method in terms of forced fluid removal, when the ultrafiltration rate significantly exceeds the plasma refill rate, there is intravascular volume depletion, which in preload-dependent HF patients can lead to a further decrease in cardiac output. In such cases, continuous ultrafiltration has emerged as a decongestion method for patients with refractory decompensated heart failure. This method enables the energetic withdrawal of isotonic fluid from the venous system under a controlled rate according to the patient’s vital signs. Furthermore, continuous ultrafiltration may compromise excessive neurohormonal activation .According to the available data and experiences, continuous ultrafiltration could be considered in patients with congestion refractory to intravenous diuretics and diuretic combinations, low urine output (<100 mL), impaired renal function, compromised function of the right ventricle, and frequent hospitalizations for decompensated HF. Termination of the procedure is indicated after the clinical resolution of congestion and after either persistent elevation of creatinine by more than 1 mg/dL compared to baseline or persistent hemodynamic instability ,32,33,34Nowadays, the theory that salt is universally deleterious, whereby excessive sodium may exacerbate acute heart failure and congestion, has been re-evaluated, as a restriction in salt intake seems to lead to a heightened sodium avidity signal. This results in neurohormonal activation and questionable differences in congestive symptoms. The role of chloride anion on salt-sensitive renal responses of tubuloglomerular feedback and renin release has been re-appraised , especiaHF is a systemic syndrome characterized by reduced cardiac output and/or high intracardiac pressure, compromising the heart’s ability to maintain adequate oxygenation of tissues. It is known that a failing heart relies on exogenous substrates for energy provision, resulting in ischemic injury and electrical vulnerability; thus, nowadays, the importance of dietary modification, beyond the preservation of uncontrolled weight loss, has attracted scientific and clinical interest. In the course of HF, a clinician has to face the challenge of cachexia or the obesity paradox.Cachexia is a complex metabolic wasting syndrome, characterized by unintentional weight loss of edema-free mass, anorexia, inflammation, anemia, and low serum albumin. All these are predictors of adverse HF outcomes. Potential treatments include appetite stimulants ; exercise; and anabolic agents, used in combination with nutritional supplements and anti-catabolic interventions, although the benefits and safety of these have not been proven .Once HF is diagnosed, increased body weight has been associated with lower mortality and better prognosis, while significant weight loss appears to correlate with higher mortality rates. In the case of body weight loss, the focus should be on the quality of the weight lost, and whether it is adiposity or involves muscle mass. Hence, nutritional status may explain this paradox when non-sarcopenic obesity exists or in excessive lean mass loss. The co-existence of a metabolically healthy status may multiply the protective effect of increased weight.Obesity has a prevalence of 30–40% in HF with a reduced ejection fraction (HFrEF) and 40–55% in HF with preserved ejection fraction (HFpEF), making this condition a challenge. According to the European Society of Cardiology (ESC), weight loss cannot be recommended in patients with moderate obesity, which is in line with the recommendation of the American Heart Association (AHA). In advanced obesity, weight loss manages symptoms and exercise capacity. To address this issue, in clinical practice, it is common to recommend a negative energy balance of 500–750 kcal/d or an absolute intake of 1200–1500 kcal/d for women and 1500–1800 kcal/d for men, aiming for a loss of at least 5–10% of the weight at baseline .Micronutrient deficiencies are attributed to appetite loss, diuretic use, renal dysfunction, comorbidities that induce dietary restrictions or malnutrition , and medications that alter the gut microbiome. Epidemiological studies have detected low intakes of vitamin A, calcium, magnesium, selenium, and iodine in 20–30% of HF patients, and low vitamin D intake in 75% of them. Despite the growing evidence regarding micronutrient deficiencies in chronic HF, the lack of recognized nutritional strategies remains an unmet challenge in HF research. Although omega-3 fatty acids may reduce arrhythmias, stabilize contractile heart cells electrically, and increase heart rate variability, there is no new randomized clinical trial to justify their use. Thus, there is weak evidence for the clinical use of omega-3 supplementation in heart failure patients , consideESC guidelines focus on fluid intake, weight monitoring, and excessive salt and alcohol avoidance, accompanied by the general principles of CVD prevention . A Mediterranean diet, fundamentally similar to the DASH diet, demonstrates positive correlations with HF progression in epidemiological studies, but additional RCTs/cohorts are needed ,44. In eDietary recommendations for heart failure management have traditionally focused on sodium and fluid restrictions. However, emerging data support the role of moderate sodium and fluid restriction, using a personalized approach. The use of individualized nutritional support, compared with standard recommendations, has shown effectiveness, especially in patients at high nutritional risk.


Dilated cardiomyopathy (DCM) remains an enigmatic cardiovascular disease (CVD) condition characterized by contractile dysfunction of the myocardium due to dilation of the ventricles. DCM is one of the major forms of CVD contributing to heart failure. Dilation of the left or both ventricles with systolic dysfunction, not explained by known causes, is a hallmark of DCM. Progression of DCM leads to heart failure. Genetic and various other factors greatly contribute to the development of DCM, but the etiology has still remained elusive in a large number of cases. A significant number of studies have been carried out to identify the genetic causes of DCM. These candidate-gene studies revealed that mutations in the genes of the fibrous, cytoskeletal, and sarcomeric proteins of cardiomyocytes result in the development of DCM. However, a significant proportion of DCM patients are idiopathic in nature. In this review, we holistically described the symptoms, causes (in adults and newborns), genetic basis, and mechanistic progression of DCM. Further, we also summarized the state-of-the-art diagnosis, available biomarkers, treatments, and ongoing clinical trials of potential drug regimens. DCM-mediated heart failure is on the rise worldwide including in India. The discovery of biomarkers with a better prognostic value is the need of the hour for better management of DCM-mediated heart failure patients. With the advent of next-generation omics-based technologies, it is now possible to probe systems-level alterations in DCM patients pertaining to the identification of novel proteomic and lipidomic biomarkers. Here, we also highlight the onset of a systems-level study in Indian DCM patients by applying state-of-the-art mass-spectrometry-based “clinical proteomics” and “clinical lipidomics”. Dilated cardiomyopathy (DCM) is characterized as a disorder of the heart muscle. It is distinguished by the widening/dilation of the left ventricle of the heart with left ventricular or biventricular systolic dysfunction ,2. ContrThe prevalence of DCM has not been well studied in India compared to many western countries in the world. However, the global burden of disease  data shoVirus, allergens, toxins and autoimmune responses are responsible for myocardial damage . This daGSH-Px) is a selenoprotein that inactivates peroxidase. Selenium is useful in cardiomyocytes for the function of the antioxidant defense mechanism and a deficiency of selenium can lead to DCM ..97].MRI is useful in determining chamber dimensions, wall thickness and ventricle mass. MRI is also useful in the assessment of flow rate, abnormality in wall motion, edema, fibrosis and hyperemia .Serological testing for virus by specific IgM antibody titer test can be useful in detecting viral myocarditis .This is the most definitive method for the diagnosis of DCM. An endomyocardial biopsy can diagnose patients who cannot be screened through other methods. Endomyocardial biopsy can detect various myocardial diseases . HoweverGenetic testing is now widely used in the detection of DCM. Genetic testing is crucial in the case of asymptomatic patients for better management and early intervention of subjects. Family genetic history using pedigree analysis has remained a classical approach in the diagnosis of genetic DCM. Pedigree analysis can help in the diagnosis of mutation in family-specific genes by genetic testing. However, it has remained a challenge to ascertain the specific genes causing DCM. Moreover, more than 100 genes have been reported to be involved in the etiology of DCM . CommercSeveral pathological tests in isolation or in combination are performed in order to detect the clinical severity of DCM patients  22,47,77,78,102.There are alterations in the protein content in the heart during the development of DCM. This alteration can be detected by proteomic techniques . These aBNP levels accurately diagnose DCM and heart failure. Brain natriuretic peptide can also be used to assess the effectiveness of a heart therapy [Brain natriuretic peptide indicates stress on the ventricles. Brain natriuretic peptide levels predict DCM as well as heart failure.  therapy .ST2 is a cardiac biomarker, which is a member of the interleukin-1 receptor family. ST2 is released by cardiomyocytes in stress conditions. The presence of ST2 indicates tissue fibrosis, cardiac remodeling and abnormality in the heart. ST2 can diagnose a heart abnormality at an earlier stage than the brain natriuretic peptide .Troponins T and I are sensitive biomarkers of heart failure. A modest increase in the serum level of troponins T and I predict abnormality in the heart. Most of heart failure patients have elevated levels of high sensitivity troponin in the serum .Collagen also works as heart failure biomarker. Elevated levels of collagen predict abnormality in the heart. Procollagen type III independently predicts progression of heart diseases .MMP-2, -7, -8, and -9 are found in children with DCM [Matrix metalloproteinases work as biomarkers for DCM and heart failure. Elevated levels of matrix metalloproteinase predict cardiac dilation and a decrease in ejection fraction. Elevated levels of with DCM .Under stressed conditions, activated macrophages produce galectin-3 protein. Galectin-3 protein predicts abnormality in the heart. Galectin-3 in combination with N-terminal brain natriuretic peptide (proBNP) is the best biomarker for the diagnosis of acute heart failure. It is also useful in assessing the effectiveness of a therapy in individuals with heart disease .There is no treatment available to permanently cure or ameliorate the DCM condition, but several treatment regimens are clinically practiced to restrict the progression of DCM and further reduce the symptoms. The current state-of-the-art therapeutic regimens described below aim to prevent heart failure and thromboembolism.In all etiologies of heart failure, the activation of the renin angiotensin aldosterone system (RAAS) is significant. To block this pathway, ACE inhibitors are used. These inhibitors are found to relieve dyspnea and reduce heart disease progression. ACE inhibitors work by preventing the formation of angiotensin II which is a vasoconstrictor that inhibits the hydrolysis of bradykinin, which is a vasodilator . Thus, ADiuretic drugs are useful in treating heart disease. Diuretics increase the excretion of water and salts from the body, which lowers the pumping load from the heart. These drugs work by inhibiting the antidiuretic hormone vasopressin and they work to reduce the blood pressure, swelling, and water buildup ,113. TheThese are angiotensin II receptor blocking drugs. These drugs bind to angiotensin II receptors and actively inhibit their function. Thus, arteriolar contraction and sodium retention is prevented by angiotensin II receptor antagonists .1-adrenergic receptors are found in the cells of the heart which are blocked by beta blockers [Beta-blockers are widely used to control heart disease. Beta-blockers are efficient in temporarily reducing blood pressure, angina, arrhythmia, anxiety, migraine, glaucoma, and overactive thyroid . Beta blblockers .Spironolactones are used to lower blood pressure. Spironolactones are useful in preventing heart failure and in some cases, they are also useful in managing edema. Aldosterone is present in high amounts in DCM patients, retains sodium inside the body, excretes potassium and causes baroreceptor dysfunction . MineralIn the comorbid condition of diabetes mellitus and cardiovascular disease, SGLT2 inhibitors are quite useful. These molecular inhibitors of sodium-glucose-co-transporter 2 reduce the blood glucose level by promoting the urinary excretion of glucose. The unique mode of action of SGLT2 inhibitors results in glycosuria. SGLT2 inhibitors show diuretic and natriuretic actions. These actions help in decreasing blood pressure and plasma volume. A decrease in albuminuria and the glomerular infiltration rate is also associated with SGLT2 inhibitor treatment . SGLT2 aDegraded myocardium, activated macrophages and T cells secrete tumor necrosis factor α (TNF-α) and other secreted proinflammatory cytokines to promote the progression of cardiomyopathy . The penIn patients with a history of thromboembolism, high ventricular dilation, and severe systolic dysfunction, anticoagulants are used in treatment . Blood tANP) are natural vasodilators and diuretics which are secreted by atrial myocytes in response to stretch/stress or other stimulations [Atrial natriuretic peptides (ulations . These mStem cell therapy is an exciting newer approach studied for the treatment of DCM. Autologous bone marrow cell therapy for DCM in the short term (6 months) and long term (3 years) showed beneficial results . In the Drugs undergoing clinical trials for DCM in the United States are listed in PLV is used in the treatment of DCM. It reduces heart wall pressure by resection of a portion of the left ventricle which lowers cardiac volume . PLV is LVADs are used in end stage heart failure patients. LVADs are used as a bridge to heart transplantation. Advanced LVADs can be used as a replacement of transplant .Patients with DCM have abnormal left ventricle function. A delay in conduction of the left ventricle is also associated in the prolongation of conduction of the atrioventricle. The synchrony in the function is restored by dual-chamber pacing . Single MYBPC3, in a South Asian population with heritable conditions of cardiomyopathies such as DCM or HCM and contributing to heart failure. The sample collection for the cardiomyopathy investigation was carried out in hospitals in Madurai, Trivandrum, Hyderabad, Kozhikode, Chandigarh, and Mumbai [TNN13 and a novel MYH7 (beta myosin heavy chain) mutation in cardiomyopathy development and a new mutation found to be associated with DCM induction [MYH7 genetic variations carried out by Tanjore et al. analyzed the mechanism behind DCM-phenotype development. The samples belonged to a hospital in Hyderabad and common SNPs were found in exons 7, 12, 19 and 20 in DCM and HCM conditions. These SNPs when present in homozygous conditions gave rise to DCM [LMNA mutations appearing in a familial DCM patient [NOS3) with three functional polymorphisms resulted in its variable expression. This led to DCM progression due to oxidative stress from the imbalanced production of nitric oxide which causes impairment in the contractile property of cardiomyocytes [EDN1) was investigated by Matsa et al. in the manifestation of DCM in 115 DCM patients from a hospital in Hyderabad, using PCR-based followed by single-stranded confirmation polymorphism analysis along with the commercial screening insertion variation (+138 A) in a heterozygotic state leading to a four-fold increased risk of DCM [TNNT)-related genetic variations were studied by Rani et al. in 147 DCM patients of south-Indian origin. Exon analysis revealed a novel mutation R144W in the tropomyosin binding domain that was responsible for distorting the protein structure and function by changing the residue charge [Several candidate-gene-based epidemiological studies have been performed in India. Most importantly, Dhandapani et al., in 2009, published a work highlighting the role of defects (25 bp deletion) in the gene myosin binding protein C in the heart represented as d Mumbai . Das et d Mumbai ,134,135.d Mumbai . They fonduction . Anothere to DCM . Similare to DCM . A first patient . Endothemyocytes . The rolk of DCM . Troponie charge . A papere charge . Similare charge . Ushasree charge . Anothere charge . A studye charge . Ahmad ee charge .So far in India, DCM has been looked at from a candidate-gene perspective. Genetic evidence from Indian populations points to the fact that the majority of the descendants of ethnolinguistic groups include a blend of various divergent ancestral natives such as those of North Indian lineage sharing kinship with West Eurasians, and Native Andaman Islanders being ancestral to Southern Indians ,155. ThiProteomic techniques combined with lipidomic concept application to study heart disease can give us new insights into the biomolecular mechanisms and changes undergone by tissue during disease progression. Our next focus in this context is to probe mass-spectrometry-based “clinical-omics” studies of DCM patients from India. This initiative has been recently funded by the Indian Council of Medical Research (ICMR). We aim to develop a noninvasive diagnostic multimarker panel (proteomic and lipidomic) that would be indicative of DCM status in Indian patients.


We aimed to evaluate the feasibility of left ventricular electroanatomical mapping to choose between left bundle branch area pacing (LBBAP) or coronary venous pacing (CVP).There are several ways to achieve left ventricular activation in cardiac resynchronization therapy (CRT): LBBAP and CVP are two possible methods of delivering CRT. However, the criteria for choosing the best approach remains unknown.A total of 71 patients with heart failure, reduced ejection fraction, and left bundle branch block (LBBB) were recruited, of which 38 patients underwent the three-dimensional electroanatomical mapping of the left ventricle to accurately assess whether the left bundle branch was blocked and the block level, while the remaining 33 patients were not mapped. Patients with true LBBB achieved CRT by LBBAP, while patients with pseudo-LBBB achieved CRT by CVP. After a mean follow-up of 6 months and 1 year, the QRS duration and transthoracic echocardiography, including mechanical synchrony indices, were evaluated.Twenty-five patients with true LBBB received LBBAP, while 13 without true LBBB received CVP. Seventeen patients received LBBAP, and 16 patients received CVP without mapping. Paced QRS duration after the implantation of LBBAP and CVP was significantly narrower in the mapping subgroup compared to the non-mapping subgroup. A significant increase in post-implantation left ventricular ejection fraction was observed in patients with LBBAP or CVP, and the mapping subgroup were better than the non-mapping subgroup. After a 12-month follow-up, atrioventricular, intraventricular, and biventricular synchronization were significantly improved in the mapping subgroup compared to non-mapping groups in both LBBAP and CVP.In our study, three-dimensional electroanatomical mapping was used to choose LBBAP or CVP for heart failure patients, which proved feasible, with better cardiac resynchronization in the long-term follow-up. Therefore, three-dimensional electroanatomical mapping before CRT appears to be a reliable method for heart failure patients with LBBB who are indicated for CRT. This study shows that three-dimensional electroanatomical mapping, with better cardiac resynchronization, provides informed guidance to choose between LBBAP or CVP for patients with heart failure. Cardiac resynchronization therapy (CRT) remains an important therapy for heart failure patients with biventricular desynchronization –3. ThereThis observational study recruited 71 consecutive patients with heart failure (HF) having reduced left ventricular ejection fraction (LVEF) and LBBB who had indications for CRT . Inclusi®, version 6, Biosense Webster Inc. California USA) or electromagnetic navigation system . First, activation mapping under sinus rhythm was performed to clarify the electroanatomical activation sequence of the left ventricle, especially the earliest and latest activation parts. Second, the potential of the His left bundle branch was mapped from the bottom to the apex of the left ventricular septum.A right femoral artery puncture and intubation was performed using the Seldinger method with an 8-Fr arterial sheath, and 35 units of unfractionated heparin per kilogram was administered. A mapping catheter  was inserted from the sheath and advanced through the aortic valve with the J curve into the left ventricular (LV). Three-dimensional electroanatomical maps of the LV were reconstructed using a non-fluoroscopic navigation system  was inserted through a fixed-curve sheath . An intracardiac electrogram was recorded from the lead tip by using the electrophysiological recording system . The tip of the mapping catheter placed in the area of the left bundle branch in the left ventricle was recorded at the right anterior oblique (RAO) 30° position and left anterior oblique (LAO) 45° as references. The sheath and lead tip were advanced to the right ventricular septum that was directly opposite the mapping catheter tip and subsequently rotated in a counterclockwise fashion so the lead tip was in a perpendicular orientation to the interventricular septum (IVS). A “W”-shaped pacing morphology in surface lead V1 was observed at this location. As the lead tip was gradually screwed into the IVS, a rightward shift of the second notch in the “W”-shaped pacing morphology could be observed. The lead tip was in the final position after a QR or rSR morphology in surface lead V1 was achieved.For patients with CVP-CRT, the tip of the mapping catheter at the area of the last activation in the left ventricle was recorded at the RAO 30° and LAO 45° positions as references. After retrograde angiography of the coronary sinus, the lateral veins or posterolateral veins that were the closest to the tip of the mapping catheter were used to target the blood vessel implanted with left ventricular lead .A pacemaker was programmed to close the pacing function of the right ventricular pacing electrode but maintain the defibrillation function. The left ventricular lead pacing was gradually prolonged until the intracardiac electrogram showed atrial sensing–ventricular sensing. The atrial-ventricular delay (AVD) was shortened by 10-ms steps, and the ECG QRS duration was the narrowest. The corresponding AVD was optimized when the ECG QRS duration was the narrowest.Cardiac electrical synchrony was assessed using the QRS duration of a 12-lead surface ECG. The surface ECG was obtained before and after the implantation. The QRS duration was measured from the onset of the intrinsic or paced QRS to the end of the QRS complex in all 12 leads. The left ventricular electrical synchrony was assessed using the LV activation time (LVAT), which was estimated by measuring the time from the intracardiac pacing spike to the R-wave peak of the QRS complex in lead V5 and V6. The widest-paced QRS duration and the wider LVAT were adopted for analyses. Two independent, experienced ECG specialists, blinded to the study, measured these two parameters.A Vivid E9 Doppler echocardiography  with M5S and 4V probes was used, with an emission frequency of 2.5 MHZ. The echocardiography examination was performed by the same echocardiologist, who was blinded to the study groups. The following indicators before and after the CRT operations were measured in the patients: the left ventricular ejection fraction (LVEF); the atrioventricular synchronous index: EA peak distance (E/A pd); the interventricular synchronous index: interventricular mechanical delay (IVMD); and the left ventricle synchronous index: standard deviation of Ts of 12 LV segments (Ts-SD12).The NYHA classifications were measured. Adverse events during the follow-up were recorded, including rehospitalization due to heart failure or death of the subjects, and the medical expenses essential for the mechanical treatment of chronic heart failure for the patients in the study group were also accurately recorded.All patients underwent transthoracic echocardiography performed by an experienced specialist who was blinded to the study at the baseline as well as the 6th-month and 12-month follow-ups. The echocardiac measurement indicators, mentioned above, were recorded. Lead parameters, including R-wave amplitudes, capture thresholds, and pacing impedances were measured 1 week after the implantation.t-test) was adopted; if not, the non-parametric test (Mann–Whitney U-test) was used to compare numeric variables. Data at the baseline and follow-ups were compared by paired Wilcoxon signed rank tests. All statistical analyses were performed using SPSS 21.0 . The P-value statistical significance threshold was 0.05, two-tailed.The continuous variables were presented as means ± standard deviations (SDs), and categorical variables were expressed as frequencies and proportions. Chi-square tests were used to compare categorical variables between the two subgroups. If variables were normally distributed, the parametric test  and no mapping subgroups . Furthermore, the paced QRS duration exhibited a significant difference between the mapping and no mapping subgroups . In the CVP group, paced QRS duration 1 week after the implantation was significantly narrower than the baseline in the mapping  and no mapping subgroups ; paced QRS duration showed a considerable difference between the mapping and no mapping subgroups . The reductive value of QRS duration from baseline to post-operation was significant only in the CVP mapping and non-mapping groups . In the LBBAP no mapping grouping, the LVEF and the intraventricular synchronization index Ts-SD12 significantly improved when compared to the baseline . Between the two subgroups, there were significant differences in LEVF, IVMD, and Ts-SD12 . In the 12 month follow-up, echocardiography parameters including LVEF, atrioventricular synchronization index EA/RR, biventricular synchronization index IVMD, and intraventricular synchronization index Ts-SD 12 were significantly improved when compared to the baseline data in the mapping subgroup . LVEF, IMVD, and Ts-SD12 significantly improved when compared to the baseline in the LBBAP no mapping subgroup . Furthermore, the LVEF, EA/RR, IVMD, and Ts-SD 12 exhibited a significant difference between the mapping and no mapping subgroups . The LVEF and IVMD were significantly improved when compared to the baseline in the no mapping subgroup ; and there was a great disparity in LVEF, EA/RR, IVMD, and Ts-SD 12 between the mapping and no mapping subgroups . At 12-month follow-up, the LVEF, EA/RR, IVMD, and Ts-SD 12 were observed to have significantly improved when compared to the baseline data in the mapping subgroup ; LVEF and IMVD were substantially improved when compared to the baseline in the LBBAP no mapping subgroup . In addition, the LVEF, EA/RR, IVMD, and Ts-SD 12 exhibited a significant difference between the mapping and no mapping subgroups . After the mapping, protamine was given to neutralize the heparin (1 mg:100 IU), and the implantation of CRT was continued. Although it was not found in this study, the complications of vascular puncture and the risk of blood oozing from the pocket are theoretically increased during this step.This study was a single-center prospective study, and the sample size was relatively small. Even though our study demonstrated novel criteria for choosing between CVP or LBBAP, which is safe and feasible, larger and randomized controlled trials should be conducted to verify its long-term safety and clinical benefits.For heart failure patients with LBBB who are indicated for CRT, left ventricular electroanatomical mapping before CRT, which determines whether the left bundle branch is blocked or not, is a safe, feasible way to choose between LBBAP or CVP. The benefit of the pre-procedural mapping is that patients with intact left bundle branch conduction  are filtered out and do not receive LBBAP, as they are unlikely to benefit. In addition, the X-ray image of the mapping catheter tip at the left bundle branch area, or the latest activation area of LV can provide a positioning reference for the implantation of the left ventricular electrode into the target area.There are currently two ways to achieve left ventricular activation in CRT. One is to place a left ventricular electrode in the coronary venous pacing (CVP), and the other is to place a left ventricular electrode in the left bundle branch area.For patients with heart failure and left bundle branch block (LBBB), there is currently no research that recommends which criteria should be used to choose left ventricular pacing to achieve CRT.Further studies with larger and randomized controlled trials should be conducted to verify the findings of this study and identify the long-term safety and clinical benefits of three-dimensional electroanatomical mapping-guided CRT.The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.The studies involving human participants were reviewed and approved by the Ethics Review Board of the First Affiliated Hospital of Kunming Medical University. The patients/participants provided their written informed consent to participate in this study.JW and LZ designed and supervised the study. B-TH, JW, and L-JP performed CRT implantation and drafted this manuscript. XT performed statistical analyses. HL, W-JS, XT, CW, X-XS, RL, S-ML, Z-XL, and J-HZ followed the patients and optimized the parameters. All authors contributed to the article and approved the submitted version.This work was supported by the National Natural Science Foundation of China , Science and Technology Department of Yunnan Province , the Yunnan Provincial Youth Top-notch Talent Support Program (RLQB20200009), and Yunnan Provincial High-level Health Technical Reserve Talents Support Program (H-2019051).The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.


COVID-19 myocarditis occurs in 7–28% of patients admitted in the hospital with or without multisystem inflammatory syndrome. It may present as fulminant myocarditis. Dilated cardiomyopathy as a sequela of COVID-19 myocarditis has been reported in the pediatric population. However, to date, no case of silent COVID-19 myocarditis progressing to dilated cardiomyopathy has been reported in children. Furthermore, although newly developed hypertension as a sequela of COVID-19 infection has been reported in adults, there is no report of newly developed COVID-induced hypertension in children. We report a 3-year-old boy with silent COVID-19 myocarditis progressing to dilated cardiomyopathy and newly developed systemic hypertension.A 3-year-old boy was referred to the emergency department because of respiratory distress. The parents gave a history of SARS-CoV-2 infection in the child 5 months ago that was manifested as fever and cough, for which he was treated as an outpatient. Echocardiographic examination revealed a severe decrease in left ventricular systolic function in favor of dilated cardiomyopathy. Cardiac magnetic resonance imaging established the diagnosis of myocarditis. The patient left ventricular systolic function did not improve after 2 weeks of intravenous inotropic support. Therefore, the child was transferred to another tertiary center with extracorporeal membrane oxygenation and pediatric cardiac transplantation facilities.COVID-19 can induce silent myocarditis with progression to dilated cardiomyopathy and newly developed systemic hypertension. Thus, a thorough examination of the heart and measurement of blood pressure are mandatory in every child with COVID-19 infection. Cardiac MR is an indispensable tool in the diagnosis, follow-up, and prognostication of COVID-19 myocarditis. Moreover, four-chamber speckle tracking strain imaging showed apical rocking in all the four heart chambers in this child with opposite direction in the failed left ventricle compared with other cardiac chambers. Lastly, the presence of septal flash on M-mode echocardiography, apical rocking and prestretch–rebound stretch patterns on longitudinal strain imaging of the failed left ventricle in this child may be of predictive value for response to cardiac resynchronization therapy.The online version contains supplementary material available at 10.1186/s43044-022-00282-w. COVID-19 myocarditis occurs in 7–28% of patients admitted in the hospital with or without multisystem inflammatory syndrome (MIS) . HoweverA three-year-old was referred to the emergency department because of respiratory distress. He was a well-nourished boy with normal temperature and a respective heart rate and respiratory rate of 140 beats and 63 per minute on physical examination. His blood pressure was 135/110 mmHg. Cardiac auscultation revealed muffled heart sounds with a grade 2/6 regurgitant systolic murmur at the cardiac apex. The rest of the physical examination was unremarkable. The parents gave a history of SARS-CoV-2 infection in the child five months ago that was manifested as fever and cough, for which he was treated as an outpatient. Furthermore, he had a history of complete cardiac evaluation for a cardiac murmur, including a comprehensive echocardiographic examination by a pediatric cardiologist one year ago, which confirmed a normal structure and function and the innocent nature of the murmur. Family history was negative except a COVID-19 infection in five months ago in other family members.Cardiomegaly, pulmonary edema, and blunted costophrenic angles were evident on the chest X-ray Fig. . The eleComprehensive two-dimensional color Doppler echocardiography revealed a severe decrease in left ventricular systolic function in favor of dilated cardiomyopathy, significant left ventricular enlargement, mild to moderate holosystolic mitral regurgitation with eccentric posterolateral jet, trivial aortic regurgitation, and septal flash Fig. . Left veSpeckle-tracking longitudinal, circumferential, radial and transverse atrial and ventricular strain imaging was performed using velocity vector imaging (VVI) of Siemens Accuson SC 2000   and SARS-CoV-2 IgG and IgM antibodies were negative. Similarly, the polymerase chain reaction for other viruses, including adenovirus, enterovirus, Coxsackievirus, Epstein-Barr virus, Influenza virus, Cytomegalovirus, Human Immunodeficiency Virus, Hepatitis B and C virus, Herpes viruses were negative. The level of troponin I was normal, but NT-proBNP was elevated.To look for Lake Louise criteria of myocarditis, cardiac magnetic resonance (CMR) imaging was performed with gadolinium study and Short Tau Inversion Recovery (STIR)/T2 weighted-sequences . This evComplete workup including endocrinologic, nephrologic, neurologic, and rheumatologic causes of hypertension was performed. The only abnormal finding was significantly elevated renin . Measurement of aldosterone and angiotensin II was not available. Kidney function and Doppler ultrasound of renal arteries and veins were normal. Cortisol and ACTH were normal. The absence of left ventricular hypertrophy on CMR and echocardiography, absence of hypertension in the past medical history of the patient, and negative workup for other causes of hypertension were in favor of COVID-19-induced newly developed systemic hypertension.Intravenous infusion of Dopamine (7.5 µg/kg/min), dobutamine (7.5 µg/kg/min), and milrinone (0.6 µg/kg/min), in conjunction with aspirin at a dose of 5 mg/kg/day, were administered for the patient. The patient’s hypertension was controlled by the administration of captopril (6 mg/kg/day every 6 h) and hydralazine (0.2 mg/kg/dose every 4 h). The patient left ventricular systolic function did not improve after 2 weeks of intravenous inotropic support. Therefore, the child was transferred to another tertiary center with extracorporeal membrane oxygenation and pediatric cardiac transplantation facilities.This is the first report of silent myocarditis and newly developed systemic hypertension after SARS-CoV-2 infection in a child.Silent myocarditis has been reported in several diseases such as Takayasu arteritis, myasthenia gravis, and systemic sclerosis –13. HoweCOVID-19 infection in children is often milder than in adults . Fever aFurthermore, the similarity of pulmonary and cardiac involvement manifestations makes distinguishing the cardiac from the pulmonary causes challenging. The associated fever and cough in this child and the child's young age that prevents communication of symptoms further distract the primary care physician of attention to the cardiac problem.Moreover, while Chen et al.  reportedAlthough we performed a comprehensive strain analysis including longitudinal, circumferential, radial, and transverse strain imaging in this patient, transverse and radial strains are reported to be less reliable , 7.The presence of four-chamber-apical rocking with opposite direction of rocking in the failed left ventricle compared to the three other cardiac chambers has not been reported before. Apical rocking or transverse motion of the apex is recognized as a marker of left ventricular dyssynchrony. It has been reported as a parameter that predicts response to cardiac resynchronization therapy –22. We mMoreover, his child had prestretch and rebound stretch in the left ventricular longitudinal strain imaging. Gorcsan et al., in a study on 422 patients with heart failure, reported the presence of systolic stretch as an indicator of favorable response to cardiac resynchronization therapy in patients with a QRS duration of 120 149 ms or absent left bundle branch block . Thus, tEvaluation of left atrial strain is a necessity in patients with heart failure. It provides information regarding the left atrium's reservoir, conduit, and booster function and is considered a parameter for assessing left ventricular diastolic function. Left atrial reservoir strain of less than 23% is abnormal , 24–28.Cardiac magnetic resonance imaging is a robust gold standard tool for diagnosis, follow-up, and prognostication of myocarditis in acute, chronic, and healed states , 30. TheThis is the first case report that indicates COVID-19 can induce silent myocarditis with progression to dilated cardiomyopathy and newly developed systemic hypertension. Accordingly, this case encompasses several critical lessons for primary care physicians and pediatric cardiologists. First and foremost, a thorough examination of the heart and measurement of blood pressure are mandatory in every child with COVID-19 infection. Second, the role of cardiac MR with appropriate sequences in the diagnosis, follow-up, and prognostication of myocarditis should not be underestimated. Third, four-chamber speckle tracking strain imaging showed apical rocking in all the four chambers of the heart in this child with secondary dilated cardiomyopathy with opposite direction in the failed left ventricle compared with other cardiac chambers. Fourth, the presence of septal flash on M-mode echocardiography, apical rocking, and prestretch–rebound stretch patterns on longitudinal strain imaging of the left ventricle may be of predictive value for response to CRT in these patients.Additional file 1. Right atrial segmental myocardial transverse and longitudinal strain imaging. As shown in the clip, apical rocking is + 0.61.Additional file 2. Left atrial segmental myocardial transverse and longitudinal strain imaging. As shown in the clip, apical rocking is + 0.12.Additional file 3. The right ventricular segmental myocardial transverse and longitudinal strain imaging. As shown in the clip, apical rocking is + 0.84.Additional file 4. The left ventricular segmental myocardial transverse and longitudinal strain imaging. As shown in the clip, apical rocking is - 0.23.Additional file 5. The right atrial global and segmental ejection fraction and segmental volume changes.Additional file 6. The left atrial global and segmental ejection fraction and segmental volume changes.Additional file 7. The left ventricular global and segmental ejection fraction and segmental volume changes.Additional file 8. The right ventricular fractional area change.Additional file 9. The left ventricular fractional area change.


Previous studies of left ventricular diastolic function (LVDF) have focused on the decrease in active and passive diastolic function due to ischemic factors but have not investigated if the decrease in compliance of the coronary arteries that bypass the surface of the heart and travel between the myocardium could cause a constricting effect on the ventricular wall like that caused by myocardial fibrosis.P < 0.001). And multiple linear regression analysis showed that T was correlated with Gensini score and C-dp/dtmax . Grouping according to the site of stent implantation and the number of stents implanted, it was found out that the changes in T values before and after left anterior descending artery (LAD) stent implantation were greater than left circumflex artery (LCX) and right coronary artery (RCA) (P < 0.001). And multiple linear regression revealed a correlation between T values and stent length, ventricular stiffness, and C-dp/dtmax (P = 0.001).581 patients diagnosed with coronary heart disease (CHD) were divided into A group (patients are the control group), B group (patients with less than 50% coronary artery stenosis), C group (patients with coronary artery stenosis between 50 and 75%), D group (patients with coronary artery stenosis greater than 75%) according to the degree of coronary stenosis. The diastolic function of the ventricle is reflected by applying the relaxation time constant T value, which refers to the time between peak dp/dt and end-diastolic pressure in the left ventricle. It was concluded that there was a statistical difference in Gensini scores between patients in groups B, C and D (The decrease in compliance of the coronary arteries bypassing the surface of the heart and travelling between the myocardium would cause a constricting effect on the ventricular wall like that caused by myocardial fibrosis.The online version contains supplementary material available at 10.1186/s12872-022-02809-0. In recent years, coronary artery atherosclerotic heart disease has caused an increasement in morbidity and mortality rate and is the leading cause of death worldwide . SeveralPCI is currently the choice of treatment for patients with coronary artery disease who have severe stenosis . One stuTherefore, it is necessary to investigate if coronary atherosclerosis and the reduced compliance of coronary arteries and small vessels distributed between the myocardium caused by the implantation of stents during PCI could cause a certain constricting effect on the heart and thus affect the diastolic function of the heart, so that the changes in diastolic function in patients undergoing PCI with stents can be investigated and appropriate therapeutic measures can be taken in a timely and rapid manner to delay or prevent the onset of left ventricular diastolic insufficiency.Inclusion subjects: From October 2016 to October 2019, 581 patients diagnosed with CHD in the Department of Cardiology, Fengxian District Central Hospital, of which 318 patients underwent PCI  the diagnostic criteria for unstable angina referred to the 2007 release of the Chinese Society of Cardiovascular Diseases; (2) Doppler ultrasound examination was performed within 3 days before PCI and 1 year after the repeat imaging, and the left ventricular ejection fraction was greater than 50%; (3) complete clinical data; (4) no history of iodine allergy.Exclusion criteria: (1) patients with a combined history of acute myocardial infarction or old myocardial infarction; (2) various organic heart diseases such as rheumatic heart valve disease, cardiomyopathy, myocardial amyloidosis, ventricular wall tumor, congenital heart disease and pericardial disease as suggested by cardiac ultrasound; (3) patients with heart failure of New York Heart Association (NYHA) cardiac function class III or above; (4) patients with chronic obstructive pulmonary disease (5) patients with atrial fibrillation; (6) patients with chronic underlying diseases such as severe hepatic or renal insufficiency or severe anemia; (7) patients requiring repeat PCI; and (8) patients with co-infectious diseases.The 581 patients selected were divided into four groups according to the degree of coronary artery stenosis. Group A patients were the control group. Group B patients had less than 50% coronary artery stenosis. Group C patients had a coronary stenosis between 50 and 75%. Group D patients had a coronary stenosis greater than 75%. And control patients were selected and grouped by an age interval of 10: group 1 (45 ≤ age < 55), group 2 (55 ≤ age < 65), group 3 (65 ≤ age < 75), group 4 (75 ≤ age).Coronary angiography and stenting were performed using standard interventional techniques according to the practice guidelines established by the Chinese Society of Interventional Cardiology. Cardiac catheterization and hemodynamic measurements were performed using a large C-wall digital subtraction X-ray system  and its matching polysomnography. Coronary angiography was performed by an experienced associate chief cardiologist or above, using multiple projections. And two experienced cardiac catheterists quantitatively evaluated the presence or absence of stenosis and vascular stenosis, selected for stent implantation according to the degree of coronary lesion, and collected the length and number of stents in patients with stent implantation. The successful PCI refers to: residual coronary stenosis < 10% after stent implantation, and visualized after angiography Assessment without significant intimal tears, distal embolism, coronary slow flow, occluded side branch occlusion. Gensini scoring method: all patients were scored for each patient's coronary lesion using the modified Gensini score under American Heart Association criteria .Left ventriculography: Patients were instructed to assume a right anterior oblique position, photographed at a 30° angle and the contrast agent iodixanol was injected at a certain rate using a high-pressure syringe, with 50 frames/s as the filming speed for coronary angiography in patients with coronary artery disease. Measurements were made according to the playback. The electrocardiogram, left ventricular pressure curve and aortic pressure curve are also recorded simultaneously for at least 5 consecutive cardiac cycles.u, Pressure upper limit; Pl, Pressure lower limit; t, time of pressure changes between P1 and P2).Measurement of left ventricular diastolic function indicators: maximum left ventricular filling rate (PFR), maximum rate of left ventricular pressure rise (LV+dp/dtmax) and maximum rate of left ventricular pressure fall (LV-dp/dtmax), systolic + dp/dtmax and diastolic-dp/dtmax, and left ventricular isovolumic diastolic relaxation are measured according to the left ventricular pressure curve using a pressure guidewire system. Time constant of relaxation  refers to the time between the peak dp/dt and the end-diastolic pressure of the left ventricle.The inverse of the slope of this line is T, which reflects active left ventricular diastolic function –16. The Coronary 64-layer spiral CT: A retrospective cardiac gated spiral scan was performed using a Philips Brilliance 64-layer CT machine to select an appropriate scan protocol. After the scan, 20  ECGs were obtained by automatic offline reconstruction using 5% intervals with a reconstruction layer thickness of 1.5 mm and a spacing of 1.0 mm, Kemal value  B26f.  cardiac cycles. The reconstructed images were transferred to the Syngo workstation, and the 5–100% full-phase images were transferred to the Circulation software for analysis of cardiac function. 21 time-phase reconstructions were transferred to the post-processing workstation, where two experienced image physicians were selected to perform post-processing and calculate left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), and left ventricular systolic volume (LVESV). End-diastolic volume (LVEDV), left ventricular systolic volume (LVESV), maximum rate of left ventricular pressure rise (LV+dp/dtmax), maximum rate of left ventricular pressure fall (LV-dp/dtmax), maximum left ventricular filling rate (PFR), and left ventricular ejection fraction (LVEF).2 tests for categorical data were used to compare if there were differences in LVDF among groups. All analyses used SPSS software version 25.0 and figures used GraphPad Prism 8.4.3. The statistical significance of all the analyses was drawn at a 2-sided significance level, which was 0.05.Baseline demographic data and clinical variables were summarized with continuous variables and expressed as mean ± standard deviation or median with interquartile range. Categorical data were expressed as percentages and number of events. ANOVA or Kruskal–Wallis non-parametric tests for continuous variables as applicable, and χp < 0.001) was found that the T values of patients in the different age groups were of statistical values with an increase in the T value of the corresponding diastolic function index as the age of the patients increased . As the degree of coronary artery disease increased, a comparison of DT and LAD measured by echocardiography and T values measured by invasive catheterization, which more accurately reflect the diastolic function of the left ventricle, revealed that patients in groups C and D where the degree of coronary stenosis was greater than 50%, showed a more significant decrease in diastolic function than patients in groups A and B. Patients in group D had poorer diastolic function than those in group C. Correlation analysis of patients in group D with T as the dependent variable showed a correlation between T and Gensini score and C-dp/dtmax  and multiple linear regression analysis showed a linear correlation between T and Gensini score and C-dp/dtmax . 0.711, B = 0.575, − 0.197, P < 0.001). As the degree of coronary atherosclerosis increased, the patient's left ventricular diastolic function also progressively decreased.581 patients were analyzed by a complete data set including LV diastolic function assessed at baseline and follow-up . T, K, LV + dp/dtmax and LV-dp/dtmax were higher than those before stent implantation and the difference was of statistical significance. Diastolic function decreased further, and diastolic function indicators gradually recovered after 1 year postoperatively , whereas the correlation between T and stent length for patients with LCX and RCA implantation had no statistical significance  , and a two-way comparison between the LAD, LCX and RCA groups revealed that the differences in T values in groups I, II and III had statistical significance. The difference between the LAD, LCX and RCA groups was statistically significant (LSD: P < 0.01). The T value of the left ventricular diastolic function index increased with increasing stent length. The degree of deterioration of LVDF gradually increased  Fig. a; after sed Fig. b.Fig. 4SP < 0.001; T-value F = 11.834, P < 0.001) . The correlation is that the longer the stent length is, the greater the increasement in LV diastolic function after PCI is. The longer the stent length, the worse the LV diastolic function after PCI   Fig. .Fig. 6ROP < 0.001). Further grouped patients undergoing PCI showed that diastolic function decreased significantly in the immediate post-PCI period in patients with LAD lesions, whereas there was no significant decrease in diastolic function in patients with LCX and RCA lesions. With the number of stents implanted increased, T values also increased. The total length of the stent implanted was positively correlated with the T value, which shows that the longer the length of the stent implanted is, the worse the patient's diastolic function in the immediate postoperative period is. But when coronary angiography was repeated 1 year after stent implantation, the T value of the patient's left ventricular diastolic function was found to have recovered.The data were collected and analyzed from 540 PCI patients and the data showed that, excluding other factors, the diastolic function index T increased with age, and the diastolic function of patients decreased (Pearson R = 0.696, Diastolic heart failure is a common clinical syndrome. The prevalence is increasing because of an ageing population and increasing co-morbidity burden. More than half of patients with exertional dyspnea of unknown origin assessed invasively have diastolic heart failure, and more than 70% of heart failure patients over 65 years old have diastolic heart failure –21. LeftCoronary atherosclerosis is caused by the accumulation of LDL to form lipid plaques, and the narrowing and narrowing of the lumen is accompanied by a hardening and loss of elasticity of the vessel wall. The degree of coronary artery disease has been shown to correlate with left ventricular diastolic function , 23, 24.Previous studies have done some comparison on LVEF for patients undergoing PCI using echocardiography before, 1 day after and 3–6 months after the procedure. It was found that LVEF improved significantly at 1 day and 3–6 months after the procedure, whereas diastolic function improved at 1 day but did not change 3–6 months after the procedure . Other sThis study had some limitations. First, the patients selected were limited to Fengxian District Central Hospital and not randomly selected patients across the country; second, the study was retrospective and not prospective. Therefore, the effect of stent length and stent implantation site on post-PCI needs to be further investigated.In this study, by comparing patients with different degrees of coronary artery stenosis, it was verified that coronary atherosclerosis can lead to a decrease in compliance of the coronary arteries travelling on the surface of the heart and the small vessels distributed between the myocardium, and it was also found that as the degree of coronary stenosis increased, LV diastolic function gradually decreased; and by further investigation, it was found that the degree of LAD vessel lesion and the LAD stent implantation were closely related to the degree of reduction in LV diastolic function. The discovery could provide new clinical ideas for active intervention in postoperative patients with cardiovascular events such as diastolic insufficiency, and also provide some clinical evidence to help clinicians better judge the application of stents in patients who need to undergo PCI length.Additional file 1: Fig. S1. The figure S1 is a supplemental data to Fig. Table S1 Single stent—left ventricular diastolic function data. To investigate the effect of stenting site on left ventricular diastolic function. According to the stent implantation site, patients implanted with a single stent were grouped and compared their LV diastolic function preoperatively, immediately postoperatively and one year postoperatively. Table S2 LAD single stent vs LAD multi-stent immediate post-operative data. To investigate whether T values are related to the number of stents implanted by comparing LV diastolic function indices in the immediate postoperative period in single versus multi-stent patients with LAD implantation.


Background: Cardiac resynchronization therapy (CRT) is a treatment for patients with heart failure and electrical dyssynchrony, i.e., left bundle branch block (LBBB) ECG pattern. CRT resynchronizes ventricular contraction with a right ventricle (RV) and a left ventricle (LV) pacemaker lead. Positioning the LV lead in the latest electrically activated region (measured from Q wave onset in the ECG to LV sensing by the left pacemaker electrode [QLV]) is associated with favorable outcome. However, optimal LV lead placement is limited by coronary venous anatomy and the inability to measure QLV non-invasively before implantation. We propose a novel non-invasive method for estimating QLV in sinus-rhythm from the standard 12-lead ECG.Methods: We obtained 12-lead ECG, LV electrograms and LV lead position in a standard LV 17-segment model from procedural recordings from 135 standard CRT recipients. QLV duration was measured post-operatively. Using a generic heart geometry and corresponding forward model for ECG computation, the electrical activation pattern of the heart was fitted to best match the 12-lead ECG in an iterative optimization procedure. This procedure initialized six activation sites associated with the His-Purkinje system. The initial timing of each site was based on the directions of the vectorcardiogram (VCG). Timing and position of the sites were then changed iteratively to improve the match between simulated and measured ECG. Noninvasive estimation of QLV was done by calculating the time difference between Q-onset on the computed ECG and the activation time corresponding to centroidal epicardial activation time of the segment where the LV electrode is positioned. The estimated QLV was compared to the measured QLV. Further, the distance between the actual LV position and the estimated LV position was computed from the generic ventricular model.Results: On average there was no difference between QLV measured from procedural recordings and non-invasive estimation of QLV (Conclusion: Using the standard 12-lead ECG and a generic heart model it is possible to accurately estimate QLV. This method may potentially be used to support patient selection, optimize implant procedures, and to simulate optimal stimulation parameters prior to pacemaker implantation. Cardiac resynchronization therapy (CRT) is a treatment option intended for patients with heart failure and reduced ejection fraction (HFrEF) and wide QRS on the electrocardiogram (ECG) . The theInverse ECG computer modeling is a means for relating ECG signals measured on the body surface to the cardiac electrical activation through equations governed by physical laws. Computing the ECG from a cardiac activation pattern is termed the forward problem, while going from ECG to myocardial activation is termed the inverse problem, or often simply electrocardiographic imaging (ECGi). The inverse problem in electrocardiography cannot be solved uniquely, and generally recordings from much more than the 10 electrodes used for measuring the 12-lead ECG are used when solving the inverse problem. Such recordings are termed body surface potential maps (BSPM). A computationally efficient way of solving the inverse problem is to define a fixed set of activation sites and minimize the error between simulated and measured ECGs or BSPMs . Given fIn this study we use an inverse ECG algorithm together with a generic geometric model and the standard 12-lead surface ECG to estimate the activation sequence of the heart for LBBB patients. Further, we estimate QLV from a given anatomical location and compare with procedurally measured QLV in patients with sinus rhythm and LBBB undergoing CRT implantation.The study population consisted of 182 patients included in the Empiric Versus Imaging Guided Left Ventricular Lead Placement in Cardiac Resynchronization Therapy (ImagingCRT) study ; a double-blinded, randomized controlled trial. The design and results of the study have previously been published , 2016. BThe included 135 patients all had simultaneous 12-lead surface ECG and bipolar right ventricular (RV) and LV pacing lead electrograms measured at the final implant site. Data was exported as two paired files per patient, one with the 12-lead ECG, and one where lead V1 was exchanged for the bipolar LV sense signal (ECG/LV). QRS duration was measured manually by one reviewer (C.G.) with digital calipers on the ECGs with magnification 200%, and the QRS onset and offset points were transferred to the ECG/LV files. QLV was then measured on the ECG/LV files by two reviewers (C.G. and J.M.), also using a digital caliper at a magnification of 500%. Any discrepancies were resolved by consensus. AHA17 segment location  for the x = 0 mm and y = 15 mm , with the catheter electrodes placed approximately 40 mm away from this origin. We first computed the activation map analytically with a conduction velocity of 0.6 m/s. Then, with a time sampling of 0.1 ms, we computed the total solid angle  at the catheter tip, all EGMs were first classified as one of the four phenotypes, and based on this configuration the QLV was determined accordingly.The Mapper is a modeling approach that aims to estimate the cardiac activation initiated from the His-Purkinje system by optimizing a forward solution to best match the ECG. The mapper has previously been validated using both endocardial and epicardial recordings , and hasThe fastest route algorithm is used to compute the activation propagation from the initial sites of activation . The fasThe geometric model used in this study to estimate the cardiac activation is from a 58-year-old male which we find to have typical body build and heart orientation. The source method used to simulate the equivalence of the cardiac activity is the equivalent dipole layer (EDL) . This moTo estimate the His-Purkinje activation sequence from a patient’s ECG, an initial activation sequence is generated to simulate ECG signals. This initial sequence uses six different anatomical locations of potential Purkinje activations sites , based qThe initial timing of each of these six locations depend on the morphology of an ECG waveform and they are used as an initial guess for subsequent iterative optimization procedures. For normal ECG morphology, the initiation times of the left septal wall was set to 0 ms, i.e. equal to the QRS onset, while the RV and LV initiation times are set to 15 ms. For ECGs with an LBBB pattern (QRS duration >120 ms) the initial timing of the left regions, is delayed to 40 ms for the septal regions and 45 ms for the free wall regions. Similarly, for RBBB ECG waveforms (QRS duration >120 ms), the initial activation of the RV septal region is set to 45 ms, and the RV free wall to 65 ms.In the subsequent optimization procedure, the timing and position of these six early sites of activation can be changed to obtain the best match between the simulated ECG and measured ECG. The total activation duration for each constructed sequence is matched to the QRS duration by adapting the overall used propagation velocity. The used propagation velocity is maintained within the physiological range of the myocardial velocity, i.e., between 0.6 and 0.85 m/s .For each patient, the mapper estimates the activation sequence of the heart based on the 12-lead ECG. The mesh-model of the heart is divided into the AHA 17 defined segments on a node level, and the geometric mean of the segment containing the LV pace electrode is computed. Since the pacing site within an AHA 17 segment is not known, we set the LV pacing site to be in the center of the myocardial segment assessed by cardiac computed tomography. The estimated activation time at this location is found by linear interpolation within the triangle encompassing the geometric mean of the segment. The time difference between the measured and estimated activation time, denoted From the estimated activation of the whole heart, we also determined the distance between the LV electrode position (defined and computed as above) and the closest point which is estimated to activate at the measured QLV time. This is done by first searching for the nearest triangulated surface element containing an activation time equal to the measured QLV. For this triangular element, the precise location activating at this time is found by linear interpolation within the triangle. All distances between points are given in millimeters. Finally, we compared the segment of the estimated QLV position to the segment containing the LV lead. We report the fraction that is placed within the same segment.Continuous variables are reported as mean ± SD unless severely skewed. Categorical values are reported as absolute numbers and percentages. For analysing associations, unpaired Baseline patient characteristics are shown in On average there was a small and not statistically significant difference between measured and estimated QLV . However, the location of LV pacing site was known with segment-level precision; LV pacing site was always placed in the segment center. For reference, in the generic model, the mean epicardial area of the defined segments is 601 mmWe presented four phenotypes of bipolar electrograms and show from a theoretical standpoint how local activation should be measured differently in the four situations. To our knowledge, such categorization and presentation is novel.Since we are using a generic geometry with uniform conduction velocity for the whole heart, it is not always possible to match the ECG exactly. One measure of the goodness of fit for the model is the error in matching QRS duration  and have areas of myocardial scarring. Especially scarring is a poor tissue substrate for stimulation and should be avoided. In the present study we used a generic model and did not take ischemia or scarring into account. However, the precision was practically the same whether patients were considered to have ischemic heart disease or not  conduction velocity. On this basis, the Mapper tries to match both the activation pattern (as governed by correlation between measured and simulated ECG) and QRS duration . Hence, it may be necessary to make a trade-off between the two. This is especially true in cases where the generic geometry is a poor match for the actual heart, and in cases where ischemia or scarring results in non-uniform conduction velocity. The limitation in the number of possible activation sites are most important in cases with complex activation sequences, where they may limit the accuracy of the solution.We demonstrated a novel non-invasive method for estimating QLV, based on the standard 12-lead ECG. On average, the method estimates myocardial activation and QLV with a small error, and may potentially be used to support patient selection, optimize implant procedures, and to simulate optimal stimulation parameters before the procedure. The use of a generic model has limitations that in some cases lead to considerable errors. This has to be taken into account when using The Mapper. Adding patient specific data, like electrode positions and body build might be necessary.


Image guidance to assist left ventricular (LV) lead placement may improve outcome after cardiac resynchronization therapy (CRT), but previous approaches and results varied greatly, and multicenter feasibility is lacking altogether.We sought to investigate the multicenter feasibility of image guidance for periprocedural assistance of LV lead placement for CRT.In 30 patients from 3 hospitals, cardiac magnetic resonance imaging was performed within 3 months prior to CRT to identify myocardial scar and late mechanical activation (LMA). LMA was determined using radial strain, plotted over time. Segments without scar but clear LMA were classified as optimal for LV lead placement, according to an accurate 36-segment model of the whole heart. LV leads were navigated using image overlay with periprocedural fluoroscopy. After 6 months, volumetric response and super-response were defined as ≥15% or ≥30% reduction in LV end-systolic volume, respectively.Periprocedural image guidance was successfully performed in all CRT patients . LV leads were placed as follows: within (14%), adjacent (62%), or remote (24%) from the predefined target. According to the conventional 18-segment model, a remote position occurred only once (3%). On average, 86% of patients demonstrated a volumetric response (mean LV end-systolic volume reduction 36 ± 29%), and 66% of all patients were super-responders.NCT05053568).On-screen image guidance for LV lead placement in CRT was feasible in a multicenter setting. Efficacy will be further investigated in the randomized controlled ADVISE (Advanced Image Supported Lead Placement in Cardiac Resynchronization Therapy) trial (  Patients with a class I and class IIa guideline indication for a de novo CRT implantation were eligible.P < .05). For late mechanical activation (LMA), feature tracking postprocessing of the cine sequences was used to determine myocardial deformation in the radial direction. As a means of enhancing interpretability and improving signal-to-noise ratio, the magnitude of radial deformation was calculated and projected, over time, on geometrical 2-dimensional (2D) and 3-dimensional (3D) cardiac models. This resulted in 4-dimensional mechanical activation plots (4D-MAPs), in which the radial strain amplitude is displayed over time. Sites of LMA were identified as having the latest high radial strain amplitude, as displayed in a patient-specific fashion  were acquired, as previously described. fashion ; Video 1Earlier image-guided LVLP studies used the 16-segment American Heart Association models.The preprocedural CMR-derived 3D LV surface models were superimposed on live fluoroscopic imaging . To this end, both a 3D and 2D technique can be used. Because 3D methods impose excessive radiation burden and are not available in all operating theaters, an easy-to-use 2D image registration technique to register the 3D LV surface model was developed. The 3D and 2D fusion techniques were evaluated for noninferiority in the first 5 patients of this study . Upon vaIn brief, EP Navigator  and CART-Box Suite Light (CART-Tech BV) were used. Periprocedural 3D CMR to 2D fluoroscopy registration was performed using 2 separate 2D fluoroscopic registrations. Here, 2 acquisitions of the LV and coronary venous anatomy were acquired during balloon occlusion and contrast infusion, using an offset of at least 60 degrees . Image fusion was performed using anatomical landmarks . The imaImplantations were performed according to local protocols, always using quadripolar leads . There wP = .536), confirming the necessity of the latter registration technique.Final LV lead positions, relative to the predefined target, were determined at the end of the study by 2 observers blinded to targets, patient characteristics, and outcome. Because defining final LV lead position is unreliable using fluoroscopy only,t test or Mann-Whitney U test, where appropriate. Fisher's exact test was used to compare nominal variables. One-way analysis of variance was used to compare 3 categories of lead locations. Interobserver reliability was determined using the intraclass correlation coefficient, or Cohen’s κ for categorical variables. All statistical tests performed were 2-tailed, and a P value <.05 was considered statistically significant.Statistics were performed in SPSS version 26 . Depending on normal distribution, continuous data were expressed using mean ± SD or as median and IQR. Categorical data were expressed as the absolute number of occurrences and associated frequency. Independent subgroups were compared using a A total of 87 de novo CRT patients were screened. Four were excluded because a contraindication for CMR  and 53 because of no consent, permanent atrial fibrillation, or no available CMR. Thirty consecutive patients were included and underwent CRT implantation between December 2019 and May 2021. One patient had no suitable venous anatomy and required epicardial lead placement, resulting in exclusion from further analysis. All 29 remaining patients successfully underwent periprocedural image guidance . Scar bu2 vs 4840 ± 2625 μGy/m2; P = .299).Complete CMR analysis was completed within 2 days after receiving data from participating hospitals. Image fusion at the catheter laboratory was performed in 22 ± 7 minutes for 3D fusion and within 5 minutes for 2D fusion. According to operating physicians, image fusion was displayed on time in 28 (96%) cases, thereby not significantly postponing LVLP. Average duration of LVLP was 50 ± 35 minutes, with a total procedure time of 120 ± 45 minutes. On average, 55 ± 28 mL of contrast fluid was used. Radiation dose area was lower using the 2D fusion method as compared with using the 3D rotational fluoroscopy (2805 ± 4051 μGy/mP < .001).Based on the 36-segment model, interobserver comparison reproduced the exact same primary target selection in 12 (63%) cases and an adjacent one 6 (32%) times. There was substantial agreement when evaluating final LV lead location categories, based on the primary target of the 2 different observers  or 3% (n = 1) of patients, respectively. Documented explanations for deviation of the advised primary target were lack of venous access (n = 5), high pacing thresholds (n = 2), phrenic nerve stimulation (n = 1), or unstable lead position (n = 1).P = .793). When separated at the median, high vs low Q-LVsense/QRSd was not associated with ΔLVESV . Pacing thresholds at the final electrode were 0.9 ± 0.5 V. At 2-month and 6-month follow-up, the 2-month biventricular pacing percentage was on average 95 ± 13% (<95% in 4 patients). No LV pacing vectors were altered and no shocks were delivered.Q-LVsense of the stimulation electrode (average 157 ± 35 ms) was similar when stratified to lead position  and unaffected by presence of scar . IntrinsP = .158) or non-LBBB and LBBB  was nonsignificantly different.In total, average reduction in LVESV was 36 ± 29%, with 25 (86%) patients being volumetric responders and 19 (66%) super-responders A. VolumeP = .796). Absolute LVEF increased on average by 13 ± 12%, with 45% of patients having their LVEF increased to ≥35% (P < .001). Log-transformed NT-proBNP decreased significantly at 2-month follow-up , with a nonsignificant trend between NT-proBNP and lead position   C.Table 2Before image guidance, the brief user questionnaire revealed a mid-(antero)lateral position as most frequently preferred target by the physician. The 4D-MAP analysis identified a target adjacent or remote from the physicians’ target in 39% and 33% of cases, respectively. Implanting physicians noted that image guidance significantly altered the implantation by navigating toward another target in 38% of cases. In 19% of all cases, another vein was chosen. They noted that the procedure was either somewhat prolonged or shortened in 21.7% and 13.0%, respectively. Ultimately, image guidance was perceived as helpful in 60.7% of cases.We demonstrate the use of image-guided LVLP in a multicenter setting, using an accurate 36-segment model. Within- or adjacent-from-target LVLP occurred in 76% of cases, with 86% of patients classified as responders. However, according to the 18-segment model, only 1 patient had the LV lead implanted in a truly remote position. Model-to-image fusion, combining CMR and live dual-view fluoroscopic venograms, is therefore feasible in a multicenter setting.There were 4 patients in our series who did not respond to CRT. Although patient characteristics also determine response to CRT, a poor LV lead position within scar likely explained nonresponse in 2 of 4 nonresponders . Importa,One previous study required CMR acquisition and CRT implantation in a single session, complicating its use in clinical practice.,,Only 34% of the 87 screened de novo CRT patients were enrolled, in part because timely acquisition of a new CMR was not always possible. However, actual contraindications for CMR were rarely encountered. Regardless, image guidance was successfully performed in all CRT patients. Notwithstanding limited venous access or high pacing thresholds, which precluded optimal LVLP in some patients, a near-optimal position was acquired in the majority of cases. In addition, implantation times compared favorably with all previously conducted live image-guided studies.,Maximizing the Q-LVsense interval is a well-recognized strategy to enhance response to CRT. Although Q-LVsense is associated with CRT response on the group level,In theory, image guidance may be most valuable in patients with non-LBBB and ICM, as these patients typically demonstrate heterogeneous LV electrical activation, have smaller target sites, and demonstrate poorer outcome after CRT when compared with non-ICM or LBBB patients.NCT05053568) will address this important limitation.Although promising, our results should be interpreted with caution in the context of a nonrandomized design. The separately conducted randomized multicenter ADVISE (Advanced Image Supported Lead Placement in Cardiac Resynchronization Therapy) trial (Use of CMR as a radiation-free and noninvasive imaging technique to guide LV lead implantation is feasible in a multicenter setting, as 76% of leads were implanted in close proximity to the target, and 86% of patients demonstrated a volumetric response, with a mean reduction in LVESV of 36%. Accurate segmental analysis, time-dependent visualization of radial strain, and periprocedural image fusion may have contributed to these promising results. The randomized controlled ADVISE trial will further study the clinical efficacy following the present approach.Data underlying this article will be shared on reasonable request to the corresponding author.