Monitoring patients with spontaneous coronary dissection (SCAD) is critical in their care, as there are no accepted recommendations. To this end, finding clinical or imaging predictors of recurrent events in these patients is essential for predicting adverse events and guiding treatment decisions between conservative medical therapy and percutaneous coronary intervention. Myocardial injury and left ventricular function after SCAD can be variable parameters that require monitoring. Echocardiography and cardiac magnetic resonance are two useful imaging techniques to do so. This review aims to analyze previously published results on monitoring myocardial injury and left ventricular function in SCAD patients while highlighting the potential benefits of contemporary imaging techniques that could further improve patient care in the future. According to the research of Saw et al. in 2017  imaging are two of the most useful diagnostic tools available for diagnosing and following up SCAD patients. These imaging methods provide invaluable information about the structure, function, and perfusion of the myocardium that is affected by SCAD-related ischemia. They can also help detect any underlying conditions contributing to SCAD development or progression. Their high-resolution images offer a comprehensive evaluation essential in identifying potential treatment strategies and monitoring response to therapy over time.When diagnosing and monitoring SCAD, one may encounter challenges distinguishing it from Takotsubo cardiomyopathy (TC), as their features bear some resemblance. In 2017, Buccheri and Zambelli  identifiIdentifying short-term and long-term indicators of a negative outcome following treatment for SCAD patients is crucial. Studies have shown that the long-term mortality rate for those who survive SCAD is relatively low, ranging from 1.2% to 8% over 3.1–10 years . HoweverAfter suffering from SCAD, the outpatient evaluation should be personalized based on the patient's clinical status, extent and location of dissection and myocardial injury, and symptoms. The American Heart Association's position paper published in 2020  suggestsChest pain syndromes may occur during early or late follow-up after SCAD. This position paper released an algorithm to assess and treat repeated SCAD symptoms. The approach considers the type of symptoms and prioritizes accurate diagnosis and symptom relief while minimizing the risk of harm from medical iatrogenic intervention .3.SCAD is a potentially serious condition where a tear occurs within the layers of the coronary artery, leading to reduced blood flow and possible myocardial damage.The commonly used imaging methods in SCAD could be classified into two groups.1.Invasive coronary angiography is used to visualize coronary arteries and detect abnormalities, including dissections.2.Computed tomography angiography (CTA) is a non-invasive imaging method that uses x-rays to create detailed cross-sectional images of the coronary arteries. It can be used to visualize the extent of coronary artery dissection and assess blood flow.3.Intravascular ultrasound (IVUS) uses a tiny ultrasound probe attached to a catheter threaded into the coronary arteries to visualize coronary arteries.4.Optical coherence tomography (OCT) is an imaging technique that uses light waves to create detailed cross-sectional images of the coronary arteries.The first imaging group is focused on SCAD diagnostic challenges and increases awareness of the various SCAD angiographic appearances from Types 1 to 4  or positron emission tomography (PET) assesses blood flow to the myocardium and identifies areas of reduced perfusion due to SCAD.3.Echocardiography is a non-invasive imaging method that uses sound waves to create real-time images of the structure and function. It can help assess heart wall motion abnormalities and identify the presence of any fluid collection around the heart .4.Strain or myocardial deformation is a comprehensive technic for assessing global and regional myocardial function in ischemic myocardium and SCAD.According to Hayes et al. . This term covers various conditions, such as non-coronary reflux, microvascular obstruction (MVO), intramyocardial hemorrhage (IMH), and microvascular injury (MVI). Even after prompt epicardial recanalization of the infarct-related artery, CMD can still occur and increase the risk of cardiovascular events regardless of the epicardial disease status. To determine functional recovery after acute myocardial infarction (AMI), Nijveldt et al.  identifiMVO and IMH were found in the same area as SCAD involvement during angiography . Althoug4.The formation of myocardial infarct size in patients with SCAD could be a balanced process and often unpredictable in accordance with the clinical course and outcome.Due to the unique nature of SCAD and its challenges in diagnosis and management, guidelines for the usage of imaging methods to follow the infarct size may not be clearly defined.The first present small study about CMR revealed that it can be useful in confirming the diagnosis of myocardial infarction in cases where there is uncertainty . MoreoveThe occurrence of myocardial injury in SCAD, which presents as myocardial infarction, may not always be visible and depends on the type of SCAD. It is in accordance with thrombolysis in myocardial infarction (TIMI) flow and the speed of healing coronary disease. Infarct size is usually quantified semi-automatically on late gadolinium enhancement (LGE) imaging using the full-width half-maximum technique such that infarct size =  × 100. Al-Hussaini et al.  defined The results of multivariate modeling show that certain factors are associated with larger myocardial infarction size (>10% of LV mass present on LGE), specifically in cases of STEMI presentation, initial TIMI 0/1 flow, multivessel SCAD, a Beighton score of at least 4, and multivessel involvement . AccordiThe myocardial infarct size can be changeable in SCAD survivors and STEMI survivors, depending on the lumen size and coronary flow through the artery. In 2019, Jackson et al.  showed ap = 0.87), biomarkers of inflammation (including C-reactive protein), or myocardial injury  and SCD. Nevertheless, information on the application of implantable cardioverter defibrillator (ICD) therapy in this group is limited , 31. SCAIn the research of Ciliberti et al. , which iThere is a strong indication that female sex hormones are involved in the marked preponderance of SCAD in fertile women, particularly in the peripartum period. SCAD events related to pregnancy are typically seen in the third trimester or shortly after childbirth. Nonetheless, there have been instances where SCAD has been observed in the first trimester and later in the postpartum period, particularly among breastfeeding women. During the peripartum phase, when female sex hormones are at high levels, estrogen and progesterone receptors in the coronary vasculature may weaken the vascular wall and cause dissection by mediating changes in the connective tissues .5.in vivo quantification of LV function between 2 and 9 days after AMI, and revascularization and cine imaging were used to determine LV volumes and global and regional function at baseline and in follow-up (CMR was the reference standard for the ollow-up .p = 0.0094) and higher EDV  compared with female Type 1 STEMI patients  and end-systolic volume (ESV) of LV were found in SCAD patients compared with matched healthy controls . There wWhen assessing LV function, echocardiography is a commonly used and accessible diagnostic tool . In casep < 0.001) and readmission rates for heart failure  (The Spanish Registry on SCAD (SR-SCAD)  discover = 0.01) .When assessing LV function, wall motion abnormality (WMA) is one more diagnostic parameter in SCAD. Al-Hussaini et al.  discoverIn addition to LVEF and WMA, global longitudinal strain (GLS) and regional strain may be useful diagnostic parameters , 39 and 6.According to Hayes et al. , reassesRoutine invasive angiography in asymptomatic patients after SCAD is not recommended . HoweverNevertheless, for medically managed patients with SCAD involving the proximal-to-mid-coronary vessel dissections, CTA imaging can play a role in confirming healing, particularly for type 1 dissections, or when considering discontinuation of antiplatelet therapies . Cardiac7.More than 50% of SCAD patients have subsequent normalization of myocardial function, WMA, and LVEF in the follow-up assessment .It was hypothesized that SCAD could result in prolonged myocardial ischemia in the territory subtended by the dissected artery, potentially causing myocardial stunning to a greater degree than myocardial infarction. Healing of the vessels leads to improvement of the LV function . PossiblThe pathophysiological mechanism of occurrence of infarct size is not the same in SCAD STEMI and Type 1 STEMI. Kotecha et al.  found thOn the other hand, Based on the previous examples of various types and management of SCAD patients, it seems that the process of normalizing LV function could be complex and require further investigation.Nevertheless, using advanced diagnostic echocardiography techniques, such as mechanical deformation and CMR assessment, can potentially provide significant benefits in monitoring SCAD patients.8.Despite our attempts to provide a comprehensive, up-to-date summary of the relevant aspects of patient monitoring and follow-up after a SCAD event and the role of imaging modalities, we must acknowledge that the lack of prospective outcome trials or large-scale observational studies that could provide solid evidence for the clinical practice largely limits the scope of the current knowledge. Therefore, most of the current knowledge is based on smaller observational studies without a long-term follow-up. Furthermore, despite our diligence in summarizing available data, some of the pertinent research may have been unintentionally missed. These limitations call for future high-volume prospective and randomized studies of following patients with SCAD to provide high-quality evidence to inform clinical practice.9.Myocardial injury and LV function after SCAD can be variable parameters and are sometimes essential in the follow-up of patients with SCAD. Advanced echocardiographic and CMR techniques may provide an excellent opportunity to monitor myocardial scarring and LV function and help guide the management of patients with SCAD. Finding accurate prognostic diagnostic parameters for the occurrence of heart failure, malignant arrhythmias, and SCD in patients with SCAD may be of crucial importance and should be the subject of future research.


Takotsubo cardiomyopathy (TCM) is a rare stress-induced condition that appears rarely in suspected acute myocardial infarction cases. It causes unexplained left ventricular failure, but most cases are reversible with supportive treatment. In this report, we present the case of a 70-year-old female who developed acute hypotension after a laparoscopic Toupet fundoplication on postoperative day one, requiring care in the surgical intensive care unit. Following consultation with the cardiology service and further imaging and tests, she was diagnosed with TCM. This report outlines the potential mechanisms and management of TCM in the intensive care unit, emphasizing the importance of prompt diagnosis and treatment. Takotsubo cardiomyopathy (TCM) is a rare form of cardiomyopathy that occurs in 1% to 2% of patients suspected of having acute coronary syndrome (ACS) . Here, wA 70-year-old female with sinus node dysfunction status, post-dual-chamber pacemakers, gastroesophageal reflux disease, and failed lifestyle changes and conservative treatment presented for Toupet fundoplication. Her other significant medical history includes hypertension, hyperlipidemia, and chronic obstructive pulmonary disease, for which she was on 2L of home oxygen via nasal cannula. Her course of anesthesia and surgery was unremarkable. Her transthoracic echocardiography (TTE) completed eight months ago, showed normal left ventricular systolic function with an ejection fraction of 57%. However, the entire anterior septum and mid and apical inferior septum were hypokinetic. Her anesthesia was maintained with sevoflurane. During the operation, she received boluses of 40 mg of ephedrine, 800 mcg of phenylephrine, and 4 units of vasopressin to maintain a mean arterial pressure greater than 65 mmHg. Her post-anesthesia care unit (PACU) stay was unremarkable, and after three hours, she completed PACU phase one and was deemed stable enough to be transferred to the floor.On POD 1, she developed acute severe hypotension and was unresponsive to a crystalloid bolus. Her other vital signs were stable and within normal limits. However, she did endorse middle to low substernal chest pain that was initially localized but later started radiating to her left shoulder. She denied any dizziness, headache, and difficulty breathing. Her physical examination was unremarkable, with weak but palpable radial and dorsalis pedis pulses bilaterally. Her lungs were clear to auscultate, and her abdomen was soft and non-tender. There was no lower extremity edema. Her EKG showed possible anterolateral infarct and anterolateral ischemia  greater than 65 mmHg.On POD 2, the patient's troponin levels increased to 0.42 ng/ml and she required up to 0.09 mcg/kg/min of epinephrine to meet her MAP goals. By POD 3, the patient's condition had improved, and her epinephrine requirement to maintain the MAP goal began to decrease. Then, on POD 4, she no longer required epinephrine to maintain MAP goals. A new TTE was conducted, which showed that her global left ventricular systolic function remained below normal, but her ejection fraction had improved to 55%. However, her cardiac apex continued to be akinetic, with the apical septal segment and apical lateral segment severely hypokinetic. Additionally, the mid and apical inferior walls, mid anteroseptal segment, mid inferoseptal segment, and mid anterolateral segment were hypokinetic.On POD 5, the patient was deemed hemodynamically stable, and she was transferred from the SICU to the medicine wards. Her troponin levels had decreased to 0.03 ng/ml by POD 6, and she was started on metoprolol 12.5 mg twice per day. Finally, she was discharged from the hospital on POD 7.Takotsubo cardiomyopathy, a relatively newly classified cardiomyopathy, was first described in Japan in the 1990s by Sato et al. and Dote et al. ,7. OveraSince then, multiple diagnostic criteria have been launched in different countries, including the widely used Heart Failure Association of the European Society of Cardiology (ESC) criteria Table  10]. In. In10]. On an EKG, patients usually show ST-elevation, T-wave inversion, and left bundle-branch block . ImagingTakotsubo cardiomyopathy is unique among cardiomyopathies as it is mostly transient, and the affected heart has characteristic hyperkinetic basal segments with anteroseptal-apical dyskinetic ballooning of the left ventricle. It has four anatomic variants: apical ballooning, basal ballooning, midventricular ballooning, and focal ballooning of the left ventricle . InteresThe pathophysiology of TCM remains uncertain, but most evidence suggests that the sympathetic nervous system and catecholamines induced by emotional and physical stress may play an important role. Approximately two-thirds of TCM patients experience an increase in circulating catecholamines, which can lead to direct catecholamine toxicity . Paur etSurgeries, which are physical stressors, can unsurprisingly induce TCM. In fact, Templin et al. reported that surgical stressors are the second most common physical stressors to induce TCM . Case reIn the acute setting, TCM can lead to complications such as acute heart failure, cardiogenic shock with left ventricular outflow tract obstruction and non-obstruction, thrombosis, and even death. In the long run, it can recur. A cohort study conducted by Santoro et al. involving 1007 patients from the German and Italian Stress Cardiomyopathy Registry (GISCR) and 946 patients from the Spanish Registry for Takotsubo Cardiomyopathy demonstrated that the overall rate of in-hospital complications was 23.3% . FurtherSupportive treatment is usually sufficient for TCM as it is mostly transient. Left ventricle function typically returns spontaneously within 21 days of onset . HoweverDue to the moderate risk of left ventricular thrombi development, patients should receive three months of dual antiplatelet therapy . HoweverAs stress-induced catecholamines and psychiatric illness may play a significant role in TCM development, studies are being conducted to determine whether behavioral health therapy can reduce their recurrence. The prospective trial, Physical Exercise and Mental Wellbeing Rehabilitation for Acute Stress-induced Takotsubo Cardiomyopathy (PLEASE) study, will help determine if cognitive behavioral therapy and physical exercise can decrease TCM recurrence .In this report, we present the first case of postoperative TCM after an uncomplicated paraesophageal hernia repair. Takotsubo cardiomyopathy can mimic ACS and myocardial ischemia, making early diagnosis challenging. However, it should be considered a potential diagnosis for unexplained hypotensive postoperative patients, especially among postmenopausal women. Further research is needed to study the incidence, pathogenesis, and management of postoperative TCM.


Spontaneous coronary artery dissection (SCAD) could be the cause of acute myocardial infarction (AMI) and sudden cardiac death. Clinical presentations can vary considerably, but the most common is the elevation of cardiac biomarkers associated with chest discomfort. Different pathological etiology in comparison with Type 1 AMI is the underlying infarct size in this population. A 42-year-old previously healthy woman presented with SCAD. Detailed diagnostical processing and treatment which were performed could not prevent myocardial injury. The catheterization laboratory was the initial place for the establishment of a diagnosis and proper management. The management process can be very fast and sometimes additional imaging methods are necessary. Finding predictors of SCAD recurrence is challenging, as well as predictors of the resulting infarct scar size. Patients with recurrent clinical symptoms of chest pain, ST elevation, and complication represent a special group of interest. Therapeutic approaches for SCAD range from the ”watch and wait” method to complete revascularization with the implantation of one or more stents or aortocoronary bypass grafting. The infarct size could be balanced through the correct therapeutical approach, and, proper multimodality imaging would be helpful in the assessment of infarct size. Inappropriate immune response to AMI scar formation could be the explanation for future LV remodeling and the infarct scar size. Sustained inflammation after AMI leads to LV remodeling and progressive cardiac dysfunction. Increased proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukins (IL)-1β, IL-6, and monocyte chemoattractant protein-1 are strongly related to inappropriate healing of the myocardium after AMI. In patients with heart failure (HF), expression of TNF-α and tumor necrosis factor receptor (TNFR1) on activated CD4+ T cells is increased . In postMyocardial strain is one of the principles for quantification of LV function, which is feasible with speckle-tracking echocardiography ,11. The The management of SCAD has been a paradigm shift during the previous decade . The reaTo conclude, SCAD represents a significant cause of AMI with a challenging diagnostic and therapeutic approach. Multimodal imaging for the establishment of infarct size and its development is crucial.


Congenital absence or deficiency of the pericardium or hemi-pericardium is uncommon. When it happens, the protection given to the heart is greatly reduced, and blunt or penetrating trauma to the chest is transmitted directly to the heart. Valvular injuries from these traumas are however rare with a case of tricuspid valve rupture reported. Traumatic papillary muscle rupture in all patients group is also rare. Co-existing rupture of papillary muscle in patients with congenital absence of the pericardium is extremely rare. We report the rare case of a patient with deficient left hemi-pericardium who had a traumatic rupture of the anterolateral papillary muscle from a road traffic accident. Cardiac injury secondary to blunt chest trauma is quite common and may affect any cardiac structure depending on the force of impact . TraumatA 44-year-old male presented with a 3-week history of congestive heart failure, NYHA II, which rapidly deteriorated to NYHA IV. There was associated constrictive central chest pain and palpitations but no syncope or fever.He had two previous road traffic accidents both on a motor bicycle. The first was 7 months prior to presentation, when he had a blunt chest injury and a fracture of his left leg. The second was a month prior to presentation, when he sustained a dislocation to his right wrist as well as a fracture to his right radius.He was dyspneic, not pale and afebrile. He had bilateral pitting pedal edema up to the knees. Pulse rate was 102 regular non-collapsing, and blood pressure was 96/75 mmHg. The precordium was active, with the apex beat located in the sixth left inter-coastal space anterior axillary line. The first and second heart sounds were present, with an apical pan systolic murmur, which radiated to the left axilla. The respiratory rate was 20 cycles/min, with bi-basal crepitations on auscultation. The abdomen and other systems were normal. The Chest X-ray showed cardiomegaly with pulmonary plethora. The echocardiography (ECG)  showed sCardiac injury secondary to blunt thoracic trauma is quite common about 20%); however, associated valvular injury is rare with about 82 reported cases worldwide , 2. In v0%; howevTraumatic injury to the mitral valve is rare, while traumatic papillary muscle rupture  is rare,Patients with congenital absence or deficiency of the pericardium  and b arTraumatic papillary muscle rupture usually affects males between the ages of 30 and 60 years and occurs equally in all races. The heart is sandwiched between the sternum and the vertebrae, thus rendering it to any anteroposterior compression of the thoracic cage. Traumatic rupture of the mitral valve or its attachments occurs in diastole when the heart is filled and is violently compressed with pressures as high as 320 mmHg . This alThe clinical presentation depends on the severity of the injury and ranges from vague chest pains to features of florid congestive cardiac failure and maybe in any class of the NYHA. They will usually present with a mitral regurgitant murmur, especially when hypovolemia has been corrected.Investigations include a chest X-ray which may show cardiomegaly with plethoric lung fields. An electrocardiogram may show sinus tachycardia. The gold standard for diagnosis is transesophageal echocardiography which has higher resolution than trans-thoracic and can confirm the rupture of a papillary muscle.The treatment involves mitral valve replacement when there is an avulsion or rupture of a papillary muscle from the ventricular wall, or mitral valve ring annuloplasty where applicable .Congenital deficiency of the left hemi-pericardium is rare. This defect puts the heart at risk of injuries from chest trauma. One of such injuries is the rupture of the anterolateral papillary muscle of the mitral valve. We present such a case, which was managed with mitral valve replacement, with a good outcome.None declared.None.


Ankylosing spondylitis (AS) is a chronic inflammatory condition primarily affecting the spine and the joints. It also affects multiple organs in the body including the cardiovascular system. Left ventricular (LV) global longitudinal strain (GLS) is a good measure for recognizing subclinical myocardial dysfunction. This study aimed to investigate if there is sub-clinical LV myocardial systolic dysfunction present in AS patients independent of the presence of cardiovascular disease risk factors. We also aimed to see if the GLS is associated with the aortic root abnormality present in these patients.Twenty-eight AS patients (mean age 40.6±10.9 years) were investigated in this cross-sectional case-control study. The control group (mean age 45.2±5 years) comprised 26 healthy individuals. Conventional and speckle tracking echocardiography was performed for all patients. LV systolic myocardial function was assessed by systolic GLS. Aortic diameters and diastolic function were also evaluated.The baseline characteristics and cardiovascular risk factors of the case and control groups were similar and did not differ significantly. The AS patients were suffering more from diastolic dysfunction in comparison to the control group (p=0.009). We only found a significantly impaired longitudinal strain in the 3-chamber view of AS patients when compared to the control group. There was no significant association between the GLS and aortic root abnormality.Although the impaired longitudinal strain present in AS patients is not associated with the aortic root abnormality, it can be an early sign of cardiovascular involvement. Speckle Tracking Echocardiography (STE) is a post-processing computer algorithm that uses grayscale digital images to strain analysis. The grayscale digital images of the myocardium have a unique speckle pattern and the algorithm automatically subdivides regions into units of pixels tracking stable patterns of speckles. Then the algorithm measures the absolute differences by searching for the new location of the speckle patterns within each of the units. STE is used to detect subclinical LV ventricular dysfunction before the development of its clinical form with high sensitivity and accuracy.8The prominent cardiac involvement in AS patients is the inflammation in the aorta called aortitis. This condition leads to aortic root dilation and aortic valve insufficiency.3 The other cardiac manifestations of AS are left ventricular (LV) systolic and diastolic dysfunction, LV hypertrophy, atherosclerosis, and valvular diseases.Apart from the limited studies using STE in evaluating myocardial function in AS patients, whether subclinical left ventricular systolic dysfunction is present in AS patients in our population independent of the presence of CVD risk factors is not known. In this study, we aimed to address this issue and see if the subclinical LV myocardial dysfunction is associated with the aortic root abnormalities in these patients.9In this case-control study, conducted from March 2017 to March 2018, we recruited 28 patients with AS and 26 healthy individuals as controls. All cases with AS were consecutively selected from among the patients who visited the clinic of the rheumatologic disease in a tertiary care centre. The diagnosis of AS was based on the modified New York criteria for AS.Inclusion criteria were patients between the age of 18 and 65 who were referred for cardiovascular evaluation by the rheumatologist. Exclusion criteria consisted of diabetes mellitus, hypertension, chronic pulmonary diseases, dyslipidaemia, chronic kidney disease, and cardiovascular diseases (CVDs) or the consumption of cardiovascular medications. Asymptomatic individuals without a history of CVDs or risk factors were selected as controls.All the subjects were examined using echocardiography and electrocardiography (ECG) for an evaluation of their cardiac status.The echocardiography was done by a cardiologist with echocardiography fellowship using a GE Vivid 7 and assessments were done for cardiac function, valvular involvement, aortic annulus size, sinus of Valsalva size, and aortic root size and diastolic function, and speckle tracking. The ejection fraction (EF) of the LV was measured using the Simpson method and the value bigger than or equal to 55% was marked as a normal ejection fraction. The valvular evaluation was performed by colour and doppler study and valvular stenosis or regurgitation more than mild was marked significant valvular disease. All images were taken in 3 separate beats and then the measurements were averaged. For speckle tracking the frame rate was 50 to 90 frames per second and the endocardial line was defined manually. Peak longitudinal strain was evaluated in two, three, and four-chamber views, and then the global longitudinal strain was derived. Diastolic function was evaluated by mitral valve flow E-wave velocity ratio to A-wave velocity and a number less than 0.8 was regarded as grade I diastolic dysfunction; the number equal to or above 0.8 was marked as no diastolic function or pseudo-normal diastolic function.Standard 12-lead ECGs were obtained using a recorder at a paper speed of 25 mm/s and a scale of 10 mm/mV standardisation. The interpreter was a cardiologist blinded to the clinical status of the patients.2 test or the Fisher exact test were used for analysing the categorical variables. The data were analysed with the Statistical Package for the Social Science Base, version 21.0 . The level of significance was 0.05.The categorical data were presented as numbers (percentages) and the continuous variables as the mean ± standard deviation or the median (interquartile ranges 25–75%), as appropriate. The continuous variables were compared between the groups using the t-test or the Mann–Whitney U tests, as appropriate. The χTable 1)There were 26 persons (18 (69.2%) men) in the control group and 28 cases (22 (78.6%) men) in the AS group. The age of the individuals was 45.27±5.06 years in the control group in comparison to 40.64±10.94 years in the AS group. All demographic data including height and weight was not significantly different across the groups.  in AS (Ankylosing Spondylitis) group had a normal systolic left ventricular function. . The sinus of Valsalva diameter was significantly  increased in the AS patients in comparison to in the control group with a value of 3.86±0.22 cm and 2.64±0.37 cm respectively. Aortic root size and aortic annulus size were not significantly different . There was no significant valvular disease in both groups.The 3-chamber longitudinal strain was significantly  impaired in the AS group in comparison to the control group with a value of −17.11±7.17 and −20.55±1.57 respectively. The 2-chamber longitudinal strain , 4 chamber longitudinal strain  and average longitudinal strain  were not significantly different.Table 2.Grade I diastolic dysfunction (E/A< 0.8) was significantly more in the AS group with 20 (71.4%) AS patients having grade I diastolic dysfunction in comparison to 8 (31%) in the control group . Grade II and III diastolic dysfunction were not evaluated and E/A> 0.8 was marked as no diastolic dysfunction or pseudo-normal findings. The echocardiographic data of the groups are shown in Table 3. There was no significant difference in ECG findings between the two groups.ECG data are listed in 1 In this study, AS patients had increased sinus of Valsalva diameter but the difference in other aortic sizes was not significant. In a study done in Norway by Helga Midtbo and colleagues, lower global longitudinal strain was associated with larger aortic root diameters.7The most common types of cardiac involvement in patients with AS are aortic root dilation, aortic valve insufficiency, and conduction abnormalities.10 it was shown that global longitudinal strain is impaired in AS patients, and they proposed it as a tool to differentiate between radiographic axial spondyloarthritis (AS) and non-radiographic axial spondyloarthritis. They also showed that even in the absence of cardiovascular risk factors or disease there is subclinical myocardial dysfunction in these patients.10 In another study by Yan Chen and his colleagues, speckle tracking echocardiography has been proposed as a tool for early detection of myocardial dysfunction in such patients.11 Another research team in China concluded that longitudinal strain impairment can be used as an independent predictor for future major adverse cardiovascular events in AS patients.12 Selin Ozen and colleagues also demonstrated that increased left ventricular global longitudinal strain is seen in AS patients.13 Apart from subclinical myocardial dysfunction many studies have also showed subclinical atherosclerosis in AS patients.15Regarding left ventricular function, we found an impaired 3-chamber longitudinal strain in AS patients in comparison to the control group. In a similar study done by Sadık Volkan Emren and his colleagues,However, our study showed that the impaired longitudinal strain did not have any association with the aortic root abnormalities we see in these patients.1 Moyssakis and colleagues found that markers of cardiac relaxation impairment were significantly increased in AS patients in comparison to the control group and it was similar to our study results about left ventricular diastolic dysfunction.16 Also another study found that left ventricular diastolic function is impaired in AS patients.17Diastolic dysfunction was also shown to be more in the AS patients in comparison to the control group in our study which is similar to the results of the Almasi S and colleague’s study.18 although in Emren SV and colleagues’ study an exact relationship between markers of inflammation and markers of left ventricular dysfunction was not found.10The exact reason for myocardial dysfunction in AS patients is unknown, but referring to some studies on the inflammatory disease, it seems systemic inflammation may implicate myocardial function,The limitations of our study include its single-centre nature and the limited number of AS patients present. A multicentre study recruiting a larger number of patients can help in identifying any possible associations between the subclinical myocardial dysfunction in AS patients and future events in these patients.Despite confirmed aortic inflammation in Ankylosing Spondylitis, there was no association found between impaired longitudinal strain and increased aortic root diameter. Although the subclinical systolic myocardial dysfunction cannot be neglected in AS patients. Concerns should rise about both the LV diastolic and the systolic dysfunction present in these patients and their early detection to avoid cardiovascular consequences.


Acute cor pulmonale (ACP) is prognostic in patients with acute respiratory distress syndrome (ARDS). Identification of paradoxical septal motion (PSM) using two-dimensional echocardiography is highly subjective. We sought to describe feature-engineered metrics derived from LV radial strain changes related to PSM in ARDS patients with ACP of various severity and to illustrate potential diagnostic and prognostic yield.This prospective bicentric study included patients under protective ventilation for ARDS related to COVID-19 who were assessed using transesophageal echocardiography (TEE). Transgastric short-axis view at mid-papillary level was used to visually grade septal motion, using two-dimensional imaging, solely and combined with LV radial strain: normal (grade 0), transient end-systolic septal flattening (grade 1), prolonged end-systolic septal flattening or reversed septal curvature (grade 2). Inter-observer variability was calculated. Feature engineering was performed to calculate the time-to-peak and area under the strain curve in 6 LV segments. In the subset of patients with serial TEE examinations, a multivariate Cox model analysis accounting for new-onset of PSM as a time-dependent variable was used to identify parameters associated with ICU mortality.p < 0.001) and increased with associated LV radial strain . The time-to-peak of mid-septal and mid-lateral segments occurred significantly later in systole and increased with the grade of PSM. Similarly, the area under the strain curve of these segments increased significantly with the grade of PSM, compared with mid-anterior or mid-inferior segments. Severe acute cor pulmonale with a grade 2 PSM was significantly associated with mortality. Requalification in an upper PSM grade using LV radial strain allowed to better identify patients at risk of death (HR: 6.27 [95% CI 2.28–17.2] vs. 2.80 [95% CI 1.11–7.09]).Overall, 310 TEE examinations performed in 182 patients were analyzed . Two-dimensional assessment identified a grade 1 and grade 2 PSM in 100 (32%) and 48 (15%) examinations, respectively. Inter-rater reliability was weak using two-dimensional imaging alone (kappa = 0.49; 95% CI 0.40–0.58; In objectively depicting PSM and quantitatively assessing its severity, TEE LV radial strain appears as a valuable adjunct to conventional two-dimensional imaging.The online version contains supplementary material available at 10.1186/s13054-023-04716-y. Acute respiratory distress syndrome (ARDS), one of the most common causes of right ventricular failure (RVF) in intensive care unit (ICU) patients, is characterized by a diffuse acute alveolar damage associated with a pulmonary vascular dysfunction and increased pulmonary vascular resistance . Acute cIn the absence of inversed septal bulging or prolonged septal flattening, the visual diagnosis of PSM in the two-dimensional short-axis view of the heart remains challenging. Measurement of the end-systolic eccentricity index has been proposed to distinguish RV pressure from RV volume overload . NeverthWe tested the hypothesis that PSM could be accurately depicted by LV radial strain in ventilated ARDS patients, and help visual diagnosis in two-dimensional imaging. Accordingly, the primary objective of this study was to describe feature-engineered metrics associated with LV radial strain changes related to PSM in ARDS patients with ACP of various severity. Secondary objectives were to assess the clinical application and the prognostic value of PSM using LV radial strain when associated with conventional two-dimensional assessment.This is an exploratory observational prospective study performed in the ICU of two University hospitals in France between March 2020 and June 2021 during the first three waves of COVID-19 in France. Eligible patients were under protective ventilation for a moderate-to-severe ARDS related to COVID-19 and underwent serial hemodynamic assessments using transesophageal echocardiography (TEE). Patients were not studied if they had a non-sinus rhythm, a chronic heart failure, or if the quality of digitally stored two-dimensional images was not adequate for accurate LV strain tracking . The proAge, sex, Simplified Acute Physiology Score (SAPS) II, Sequential Organ Failure Assessment (SOFA) score, and comorbidities were recorded. Conventional hemodynamic and ventilatory parameters were collected at the time of TEE assessments.TEE examinations were performed in sedated patients using a Philips EPIQ7 upper-end system equipped with a X7-1 or X8-1 transesophageal probe . In the low transesophageal four-chamber view, end-diastolic RV and LV areas were measured and their ratio computed, while interventricular septal motion was analyzed throughout the cardiac cycle in the transgastric short-axis view at the level of the mid-papillary muscle at end-expiration . RV dilaConventional visual  identification of PSM was performed independently by two investigators with an advanced level in critical care echocardiography . PSM wasThe same two-dimensional digital loops were used for LV radial strain analysis. All strain measurements were performed independently by another trained operator using the QLAB 13 software . The region of interest  was manually determined and six LV segments were distinguished: mid-infero-septal and mid antero-septal, their opposite segments , and the remaining two segments (mid-anterior and mid-inferior) The time to peak occurs after the aortic valve closure in the septal segments(ii)The time to peak of septal segments occurs later than anterior or inferior segments(iii)The area under the curve during systole period increase in the septal segments.We first confirmed that LV radial strain curves were altered in certain segments when a PSM was present Fig.  and defihttps://gitlab.com/antoinehumeau/qlabraw2rectangulardata). To allow inter-individual comparisons, each measured time period was expressed as a percentage of the total length of cardiac cycle, and strain values were normalized by the maximal value measured during the cardiac cycle The “time-to-peak” defined as the time lag required to reach the maximal value of strain, which was normalized by the length of cardiac cycle and expressed as a percentage.(ii)The “partial area under segmental strain curves” which was calculated as the area under each LV segmental strain curve between 33 and 66% of the cardiac cycle length  to standardize the measurement.We then developed an R package to automatically extract the data generated with QLAB13 and converted them to a tidy data frame  using bootstrapping. Inter-observer variability for the diagnosis of RV dilatation was also assessed by intra-class correlation coefficient. We assessed the diagnostic capability of PSM to predict associated RV dilatation and calculated the sensibility and the specificity of this approach. For the survival analysis in the nested longitudinal cohort, variables identified as confounding factors were selected for multivariate analysis . A multivariate Cox model analysis accounting for new-onset of PSM as a time-dependent variable was used to identify parameters associated with ICU mortality using conventional two-dimensional assessment alone and in association with LV radial strain [p-value ≤ 0.05 was considered significant. All data were generated using R software (4.2.1). R packages used are provided in the Supplementary materials  were suitable for LV radial strain analysis. Only 6 patients (3%) were under vasopressors during the first TEE assessment  (Table p < 0.001). TAPSE and tricuspid S’ velocity were significantly decreased in patients with grade 2 PSM, but with median values within the normal range, while the systolic right ventriculo-atrial pressure gradient increased significantly with the grade of PSM , a grade 2 PSM in 48 cases (15%), and a normal septal motion (grade 0) in the remaining 162 examinations (52%). RV dilatation was present in 127 examinations (78%) , whereas it was substantially increased using associated LV radial strain visual assessment . ICC for RV/LV end-diastolic area assessment was good .The inter-observer variability for the diagnosis of PSM was weak using conventional two-dimensional assessment alone  TEE studies, initially interpreted without PSM using solely conventional two-dimensional imaging, were subsequently revised as displaying a PSM grade 1, and 8 (2.5%) as PSM grade 2 when LV radial strain was used Fig. A. LikewiGrade 2 PSM was systematically associated with the presence of severe RV dilatation   of the initial cohort with more than one TEE assessment were included in the exploratory longitudinal analysis. Characteristics of included and excluded patients are provided in the Additional file n = 3; care withdrawal: n  = 2).When studying the subset of patients with at least three TEE assessments, 50% of patients with PSM grade 2 on the third examination exhibited a PSM grade 0 or 1 on the previous ones, and almost all of them died Fig. D. Fifty This study first describes abnormal patterns of LV radial strain in ventilated patients with ARDS and associated PSM. It shows that the magnitude of the PSM could be quantitatively assessed using parameters derived from LV segmental strain curves. It confirms the high subjectivity of visual diagnosis of PSM using conventional two-dimensional imaging in this clinical setting and suggests the additional diagnostic and prognostic value of associating LV radial strain assessment.Accurate identification of PSM in ventilated ARDS patients is clinically relevant since ACP is associated with an increased risk of mortality –5 and maInterestingly, our results suggest that the additional use of LV radial strain may facilitate the diagnosis of PSM in clearly depicting abnormal segmental strain curve patterns, as illustrated in our patients with ACP. Facilitated PSM diagnosis allows to better identify patients at risk of developing a more severe form of ACP, which has been shown to be independently associated with ICU mortality , 18, 19.Other echocardiography methods have been previously proposed to objectively identify PSM, such as color-encoded automatic endocardial boundary detection . The maiClinical implication on mortality needs to be interpreted very cautiously because of the small sample size, which mainly focused on the most severe patients. Nevertheless, the present results confirm that severe ACP, corresponding to our patients with a grade 2 PSM, is strongly associated with mortality. This approach also takes into account the evolution during ICU stay, which provides a more relevant approach than an isolated TEE assessment on ICU admission , 19.In the present study, patients with a grade 2 PSM exhibited systematically a severe RV dilatation, corresponding to a severe ACP [This proof-of-concept study has several limitations. The proposed metrics have been elaborated to allow quantitative comparisons of strain indices between LV segments in a given patient, and between patients for a given myocardial region, due to large overlaps of individual values between patient groups . Nevertheless, they need to be validated in other populations at high risk of developing ACP. Rather than assessing the diagnostic capacity of cutoff values of the proposed indices derived from segmental LV strain curves, an individual machine learning predictive modeling approach would be more appropriate to best identify and quantify the presence of PSM. In addition, we purposely excluded from analysis patients with non-sinus rhythm or chronic heart failure, which are all potential confounders which presumably invalidate the proposed approach. Similarly, we did not studied patients with left bundle block branch and did not assess specifically how distal conduction abnormalities could alter segmental strain curve patterns. Nevertheless, in these patients, abnormal strain curve pattern seems to occur in early systole and apart from abnormalities related to PSM . We onlyIn summary, TEE LV radial strain allows to visually help identifying abnormal patterns of contraction of mid-septal segments in ventilated ARDS patients with ACP. Parameters derived from abnormal LV segmental strain curves could provide a quantitative assessment of the magnitude of PSM. Whether a machine learning approach could allow automated, accurate identification and quantification of PSM using metrics derived from LV strain curves analysis remains to be determined.Additional file 1. Supplementary study design and methods. Echocardiography, Supplementary Data engineering and R Packages used. Table S1. Comparison of the different strain parameters between patients with normal septal motion and with paradoxical septal motion of different grades. Table S2. Comparison of characteristics between patients included and excluded from the longitudinal analysis. Table S3. Multivariate Time dependent Cox Model Regression using assessment only with conventional two dimensional assessment alone and with the association of LV radial strain. Figure S1. Flowchart of the study. Figure S2. Boxplots with density plots comparing right ventricles parameters stratified by the grade of septal motion. Figure S3. Boxplots with density plots comparing the time difference between time-to-peak and the time of aortic valve closure in each of left ventricular segment. Figure S4. Boxplots with density plots comparing the time difference between time-to-peak of left ventricular septal segments and anterior or inferior segments in each grade of septal motion. Strobe statement. Supplementary references.


Congenital pericardial absence is an uncommon cardiac anomaly that is typically asymptomatic and commonly misdiagnosed due to a lack of symptoms or atypical symptoms. Pericardial agenesis (PA) should be considered one of the differential diagnoses when the patient presents with chest pain. This case shows how the diagnosis of pericardial agenesis is made exclusively using multi-modality imaging, starting from findings in a basic chest radiograph to cardiac MRI, while also demonstrating the classic signs seen in this condition. Magnetic resonance imaging of the heart is the gold standard for determining the absence of pericardium in the prognosis.A 32-year-old male who presented with chest discomfort and radiating pain to his back and left shoulder mimicking myocardial infarction with normal ECG and enzyme markers. A chest radiograph (taken 24 h apart) demonstrates the left lateral position of the heart and the bulging contour of the left heart border, a lucent area between the aorta and pulmonary artery. Subsequently, cardiac MRI reveals left pericardial agenesis.This article provides insight into a rare differential to consider in a young patient presenting with chest discomfort. This case shows how the diagnosis of pericardial agenesis is made exclusively using multi-modality imaging, starting from findings in a basic chest radiograph to cardiac MRI, while also demonstrating the classic signs seen in this condition. Pericardial agenesis is an infrequent heart anomaly that can be partial or complete , 2. DefeWe describe an unusual example of a total absence of left the pericardium accompanied by an atrial septal defect of secundum type (ASD).Technique: Multiplanar cardiac magnetic resonance imaging was done. Acquisitions were made in four-chamber, short-axis, and two-chamber perspectives.A 32-year-old male driver by profession presented to the cardiology department complaining of chest discomfort and a history of pain radiating to his back and left shoulder, which had gotten worse following four days of weight training. There are no comorbidities. History of similar complaints in the past with the first episode at the age of 10 years and similar such complaints are noted on lifting heavy weights, climbing uphill and on exertion. There is no history of concomitant surgical operations or substance abuse. There is no family history of ischaemic heart disease. Clinical assessment is normal. Routine blood tests and cardiac markers are normal. On presentations, vitals were heart rate of 164 beats per minute (tachycardia), blood pressure of 130/84 mmHg, and respiratory rate of 24 cycles per minute (tachypnoea), with normal blood glucose sugar level and showing normal ECG findings.The patient was directed to the radiology department for additional assessment. The chest X-ray indicated a normal apex and left heart border but a lucent region, as well as lung tissue between the left hemidiaphragm and heart base Fig. A. The paThe left inferior pulmonary vein seems to have a restricted calibre as a result of compression between the descending aorta and left atrium, most likely caused by significant levorotation Fig. A. On theInvestigations on the mobility of the walls of the left and right ventricles show excessive cardiac mobility is defined by a 1.5-to-2 mm displacement of the heart apex. The normal pulmonary artery diameter is 25 mm. The rest of the heart looks normal. Pleural or pericardial effusion is absent with normal ventricular walls Fig. . Fig. 4PA chest HRCT was performed, revealing the absence of the pericardium on the left side. Lung tissue may be recognised between the aorta and the primary pulmonary artery Fig. A. Lung tThe pericardium is a double-layered fibro-serous sac that surrounds and stabilises the heart within the thorax, preventing it from overfilling, minimising friction, and protecting it from infection by neighbouring organs. When pleuro-pericardial membranes merge in the fifth week of embryonic development, the pericardium forms. Failures of this process, which may be caused by early Cuvier duct atrophy, result in congenital abnormalities such as complete or incomplete pericardial agenesis . InadequDuring diastole, the normal pericardium is between 1.7 + 0.5 mm and 1.2 + 0.5 mm thick. Although not all pericardial recesses are visible on MRI, several are including the transverse pericardial sinus, which is dorsal to the ascending aorta, and the oblique pericardial sinus, which lies behind the left atrium. Additionally, an aberrant posture of the heart, bulging of the major pulmonary artery, and lung tissue interposition between the left hemidiaphragm and the inferior side of the heart, as well as between the great arteries, are all symptoms of a total left defect. Additionally, a herniated heart can be caused by a pericardial defect, evident in a partial defect . CT helpPatients with a full pericardial defect frequently have a favourable prognosis and are not treated until significant symptoms develop. However, in patients with partial pericardial agenesis, herniation of the heart due to tension on the chordal tissues can result in tricuspid regurgitation, catastrophic myocardial strangling, ischaemia, and sudden cardiac death. Unless complications arise, minor or full anomalies do not generally require repair. When herniation develops or is imminent in partial defects, the defect can be widened surgically by pericardiectomy or pericardioplasty . AdditioPericardial agenesis, although rare, should be considered in patients presenting with angina or discomfort radiating to the left arm. It can, however, be asymptomatic and have a varied range of symptoms. The present patient was incidentally diagnosed with pericardial agenesis at the age of 32. Cardiac MRI helps in knowing the type, axis, and other associated cardiovascular abnormalities.


Episodes of ischaemia-hypoxia in the perinatal period as well as the changes in the redistribution of blood may lead to decreased perfusion and ischaemia of the cardiac muscle. Additionally, there is a negative impact from the reduced contractility of the cardiac muscle secondary to acidosis and hypoxia. Therapeutic hypothermia (TH) improves the late effects in moderate and severe cases of hypoxia-ischaemia encephalopathy (HIE). The direct impact of TH on the cardiovascular system includes moderate bradycardia, increased pulmonary vascular resistance (PVR), inferior filling of the left ventricle (LV) and LV stroke volume. The above-mentioned consequences of TH and episodes of HI in the perinatal period are therefore exacerbation of respiratory and circulatory failure. The impact of the warming phase on the cardiovascular system is not well researched and currently few data has been published on this topic. Physiologically, warming increases heart rate, improves cardiac output and increases systemic pressure. The effect of TH and the warming phase on the cardiovascular values has a decisive impact on the metabolism of drugs, including vasopressors/inotropics, which in turn affects the choice of medication and fluid therapy.The study is a multi-centre, prospective, case-control, observational study. The study will include 100 neonates (50 subjects and 50 controls). Echocardiography and cerebral and abdominal ultrasound will be performed in the first 1/2 days after birth as well as during warming i.e., on day 4/7 of life. In neonatal controls these examinations will be performed for indications other than hypothermia, most frequently because of poor adaptation.The Ethics Committee of the Medical University of Warsaw approved the study protocol prior to recruitment (KB 55/2021). Informed consent will be obtained from the carers of the neonates at the time of enrolment. Consent for participation in the study can be withdrawn at any time, without consequences and without obligation to justify the decision. All data will be stored in a secure, password-protected Excel file that is only accessible to researchers involved in the study. Findings will be published in a peer-reviewed journal and disseminated at relevant national and international conferences.NCT05574855. HIE occurs in 3–5 of 1,000 neonates in developed countries . Despite1.1.Transitory hypoxia of the myocardium (and its resultant dysfunction), which may, but not necessarily, present clinically, occurs in two thirds of neonates born with perinatal asphyxia . There i1.2.•Moderate bradycardia resulting from the decreased effect of the parasympathetic system on cardiac function. Indeed, sinus bradycardia leads to reduced stroke volume and decreased requirement for energy by the myocardium –5. In tu•Additionally, TH leads to increased PVR, potentially resulting in a clinical picture of persistent pulmonary hypertension in the neonate (PPHN) or its exacerbation in cases of pre-existing raised PVR , 6. In a•The resulting RV dysfunction and reduced stroke capacity of the RV leads to reduced pulmonary venous return and therefore inferior filling and stroke volume of the LV. A consequence of the effects of TH mentioned above and of an episode of HI in the perinatal period is therefore exacerbation of respiratory and circulatory failure.TH improves the distant results in cases of moderate and severe HIE and is currently the standard of care for neonates born at or near term (>35 weeks of gestation). The direct effect of TH on the cardiovascular system includes the following:1.3.The impact of the warming phase on the cardiovascular system has not been well documented and currently very little data was published on this topic. Physiologically warming accelerates the heartbeat and improves stroke volume , althoug2.Haemodynamic changes were assessed by echocardiography doppler in neonates with HIE during TH and the warming phase.2.1.Assessment of left and right ventricular systolic-diastolic function during therapeutic hypothermia and in the warming phase.2.2.•Assessment of cerebral circulation in neonates and controls by Doppler evaluation of blood flow in anterior cerebral artery (ACA) and middle cerebral artery (MCA), and flow in the superior vena cava (SVC) cardiac output (CO)•Assessment of visceral circulation in neonates and controls by Doppler blood flow evaluation in mesenteric artery (SMA).•Assessment of renal circulation in neonates and controls by Doppler blood flow evaluation in right renal artery (RRA).3.3.1.This is a multicentre, prospective, case-control, observational study. The number of subjects under observation will be 100 neonates (study summery N). The study will take place in the period June 2021–June 2023. The proposed protocol of the study is shown in Images and clips from examinations conducted for indications, other than hypothermia, most frequently because of difficult adaptation, will be used for neonates in the control group  •Healthy, term neonates, who underwent echocardiography on days 3–7 of life  for reasons such as difficult adaptation, gestational diabetes of the mother etc.The study will include 100 neonates (50 subjects and 50 controls).Enrolment of patients will be based on patient medical records. Physicians responsible for recruitment of patients will gather additional information associated with the inclusion and exclusion criteria  through 3.4.All cardiac scans will be performed in standard echocardiographic projections with the aid of a sector probe with high frequency 8–12 MHz on a Philips camera. Echocardiography will be performed with continuous electrocardiography (ECG) recording from an ultrasound apparatus. Heart rate (HR) will be recorded. Doppler examination of the cerebral, renal and visceral circulation is an essential examination to assess haemodynamics and is routinely performed in ill neonates.The scans will be saved as video recordings on storage media. In order to decrease the duration of patient examination to a minimum of 10–15 min, echocardiographic measurements will be performed on the recorded film clips or in the Image Arena echocardiographic program.All parameters will be measured during end expiration and three consecutive cardiac cycles will be measured and averaged for each measurement.LV and RV systolic and diastolic function on cardiac echocardiography will be assessed using the following imaging options –13:3.4.A.E/A) ratio. MV E′/A′ ratio, SVC (CO), peak systolic velocity (S′), E′, A′, tricuspid valve (TV) early diastolic velocity/late diastolic velocity (E/A) ratio. TV E′/A′ ratio, tricuspidal annular plane systolic excursion (TAPSE), mitral annular plane systolic excursion (MAPSE), ductus arterious (DA) evaluation, tricuspidal valve regurgitation (rTV):Pulse Doppler, M-mode, Tissue Doppler (TDI) . The exa3.4.1A.Two-dimensional (2D) M-mode measurements will be obtained from a parasternal long-axis view. The following measurements will be assessed: aortic diameter (AO) at the level of the valvular annulus, LV internal diameter at end diastole (LVIDd) and at end systole (LVIDs), left atrial size, RV diameter at end diastole (RVDd), and LV posterior wall thickness at end systole (LVPWs) and at end diastole (LVPWd). Fractional shortening (FS) will be calculated (LVIDd − LVIDs)/LVIDd × 100. The ECG will be recorded continuously during the examination.3.4.2A.LVOT (ml/kg/min) = velocity time integral (VTI) × aortic area × heart rate, The ECG will be recorded continuously during the examination.Left ventricular cardiac output will be recorded from an apical 5-chamber view with a pulsed-wave (PW) Doppler with the flow volume measured in the middle of the outflow tract at the level of the ascending aorta. Aortic area will be measured in 2D echocardiography from a parasternal long-axis view. CO3.4.3A.svc (ml/kg/min) = velocity time integral (VTI) × svc area × heart rate, The ECG will be recorded continuously during the examination.Superior Vena Cava cardiac input will be recorded from subcostal coronal midsection views with a PW-Doppler with the flow volume measured in the middle of the inflow tract. SVC area will be measured in 2D echocardiography from suprasternal views. CO3.4.4A.A mitral inflow velocity pattern and tricuspid inflow velocity pattern will be recorded from an apical 4-chamber view with a PW Doppler sample volume positioned at the tips of the mitral leaflets and tricuspid leaflets, respectively. Tricuspid and mitral insufficiencies will be evaluated from the measurement of the spatial distribution of the tricuspid or mitral regurgitation jet using colour Doppler examination in the apical four-chamber view. Mitral incompetence and tricuspid incompetence will be graded as trivial, mild, moderate, and severe.3.4.5A.The AcT/RVET ratio will be measured at the parasternal short axis view with a pulsed-wave Doppler sample volume positioned at the tips of pulmonary valve: AcT-acceleration time (time to peak velocity of pulmonary blood flow), and RVET-right ventricular ejection time.3.4.6A.S), the early diastolic myocardial velocity (E), the late diastolic myocardial velocity (A) at the time of atrial contraction, and the ratio of E/A will be determined. DTI time intervals will be measured from recordings. The intervals (a) between the end of the late diastolic annular velocity and the onset of the early diastolic annular velocity will be equal to the sum of the isovolumetric contraction time (ICT), isovolumetric relaxation time (IRT), and ejection time (ET). The ET (b) will be measured as the duration of the systolic annular velocity (S). The sum of the ICT and IRT will be obtained by subtracting b from a. Then the LV MPI and RV MPI indexes will be calculated as (a − b)/b. The IRT will be measured from the pulsed-wave Doppler tissue recordings as the time interval from the end of the systolic annular velocity to the onset of the early diastolic annular velocity and the ICT will be obtained by subtracting the IRT from (a − b). The ECG will be recorded continuously during the examination.PW DTI will be performed using a special software package available on the Philips apparatus. This method is capable of providing measurements of ventricular wall motion velocity by positioning the sample volume at mitral and tricuspid valve annuli. In the apical 4-chambers view, the pulsed Doppler sample volume will be placed at the lateral margin of the mitral annulus and lateral margin of the tricuspid annulus. The systolic velocity (3.4.7A.E) and late diastolic, i.e., atrial (A) waves in m/s, will be measured with calculation of the tricuspid valve E:A ratio.Pulsed Doppler myocardial perfusion imaging (MPI) for the right ventricle. The tricuspid inflow velocity pattern will be measured from an apical 4-chamber view with a pulsed-wave Doppler sample volume positioned at the tips of the tricuspid leaflets. All parameters will be measured during end expiration and five consecutive cardiac cycles will be measured and averaged for each measurement. Diastolic flow through the tricuspid valve in the apical four-chamber view, including early diastolic (a − b)b. Doppler echo (clicks) of the opening and closing of the aorta valve (AV) and MV will be used as reference points to estimate the timing of the ejection period.RV ET will be measured separately from the parasternal short-axis scan plane with a PW Doppler signal placed at the pulmonary valve annulus in the RV outflow tract. The ECG will be recorded continuously during the examination. The calculation of the Tei index (RVMPI) will be considered meaningful for the RV if the difference in heart rate for the inflow and outflow path is 5 beats/min. The isovolumetric contraction time (ICT), isovolumetric relaxation time (IRT), and ejection time (ET) will be measured, and the MPI calculated using the formula (ICT + IRT)/ET, and calculated as (3.4.8A.E/A (positive) and the aortic (negative) blood flow waveforms. Diastolic flow through the mitral valve in the apical five-chamber view, including early diastolic (E) and late diastolic, i.e., atrial (A) waves in m/s, will be measured with calculation of the valve E:A ratio. The ECG will be recorded continuously during the examination. The isovolumetric contraction time (ICT), isovolumetric relaxation time (IRT), and ejection time (ET) will be measured, and the MPI will be calculated using the formula: (ICT + IRT)/ET, and calculated as a − b/b.Pulsed Doppler MPI for the left ventricle. The mitral inflow velocity pattern will be recorded from an apical 5-chamber view with a pulsed-wave Doppler sample volume placed below the mitral valve towards the ventricular septum with the PW-Doppler tracing including both the 3.4.B.Doppler measurements of other organs: resistive index (RI) in RRA, SMA, ACA, MCA .The resistance index has an inverse relationship with blood flow and will be calculated = (PSV − EDV)/PSV. PSV, peak systolic velocity; EDV, end-diastolic velocity. Since bradycardia can interfere with the measurement of blood flow indices: RI and PI, the authors additionally investigated half peak systolic velocity (h-PSV) deceleration time (DT) in ms, which evaluates the time that it takes a single flow velocity waveforms (FVWs) to halve its maximum systolic velocity. A perpendicular line was then drawn from the point of half the maximum velocity to the spectral waveform, which measures the deceleration time in ms  Figure 23.4.1B.The MCA travels laterally and enters the sylvian fissure and is the largest branch of the internal carotid artery supplying the basal ganglia, parietal and temporal lobes. The course of the artery makes it ideal for Doppler assessment. A sectoral transducer 8–12 MHz will be used and placed superior and parallel to the zygomatic arch with the marker directed anteriorly. The colour Doppler will be used, tilting or sliding the probe gently to identify the circle of Willis, with importance to set the colour scale low (10–20 cm/s). The MCA is seen coming directly forward. The PW Doppler cursor will be placed in the proximal portion of the MCA to obtain the velocity profile.3.4.2B.The ACA runs in the longitudinal fissure and curves around the genu of corpus callosum supplying the basal ganglia, frontal and parietal lobes. The transducer will be placed in the fontanelle in the midline with the marker directed anteriorly. The ACA will be identified using the colour box, with importance to set the colour scale low (10–20 cm/s). The Power Doppler cursor will be placed in the distal portion of the ACA in order to obtain the velocity profile.3.4.3B.The superior mesenteric artery (SMA) is the second artery arising from the abdominal aorta. The SMA supplies nearly the entire small intestine and a substantial part of large intestine. The transducer with a lower frequency of 5–8 MHz will be used, placed below the xiphoid process with the probe marker directed superiorly. A 2D image will be used to find the abdominal aorta and colour Doppler will be used to identify the celiac trunk flow and the SMA flow directed forward, but at an angle. The PW Doppler cursor will be placed in the SMA, sliding and tilting the probe to decrease the angle of insonation and to obtain the velocity profile. The SMA measurement will be performed fasting, prior to the next feeding.3.4.4B.A transducer with a lower frequency of 5–8 MHz was used. The transducer will be placed on the flank a few centimetres above the level of the umbilicus, the probe marker directed superiorly. The kidney will be identified in the long axis on 2D imaging. Blood flow from the aorta to the renal hilum will be found using Colour Doppler and the PW Doppler cursor will be placed in the RA prior to the point in which it branches in the renal hilum, sliding and tilting the probe to decrease the angle of insonation and to obtain the velocity profile.R) will be determined—as an indirect measure of the impact of random variability on the measurement results and the coefficient of variation (V) defined as the quotient of the mean of the squared differences between the pairs of measurements to the product of the standard deviations of both series of measurements. This method of calculating the coefficient of variation provides for taking into account the systematic error component.In order to assess the repeatability of the measurements, a pairwise comparison will be made between the results of 2 series of measurements performed by one researcher (N.B.) (intra-observer variability) and two researchers (N.B and R.B) (interobserver variability). On the basis of these series of measurements, the value of the Pearson linear correlation coefficient , systolic function-FS%, LVO, •S′, TAPSE, diastolic function-E:A ratio, E':A′ ratio measured on TV.RV function: global RV function-MPI , systolic function: •PPHN: AcT:RVET, TAPSE, incompetence gradient rTV + right atrium pressure•Systemic Flow (50%): SVCO•Systemic resistance: h-PSV-half peak systolic velocity, RI-resistance index in SMA, ACA, MCA, RRA3.6.To assess the hemodynamics of the circulatory system, the authors also used echocardiographic measurements, the value of which is independent of the presence of DA, PFO, HR, age, body weight, such as the TEI index for RV and LV, and used the tissue Doppler function to assess the myocardium.An additional advantage of the study is the large size of the study group compared to other publications.4.No study-related interventions are planned. All neonates will be treated according to current guidelines.5.5.1.•Assessment of the influence of TH on systolic-diastolic functions of the left and right ventricles in comparison with the control group•Assessment of the effect of the warming phase on the systolic-diastolic functions of the left and right ventricles in comparison with the control group5.2.•Assessment of the influence of TH on the cerebral, visceral and renal circulation in comparison with the control group•Assessment of the effect of the warming phase on the cerebral, visceral and renal circulation in comparison with the control groupThis study assesses the hemodynamic changes by means of echocardiographic Doppler examination in neonates with HIE during TH in the warming phase in comparison with the control group of healthy neonates.The intention is to assess the impact of TH on the cardiovascular system, including the cerebral, visceral and renal circulation.TH may have an adverse effect on the cerebral circulation by increasing vascular resistance and loss of adaptation of the cerebral vessels, which in turn can lead to hypoperfusion of vital organs.The effect of the warming phase on the cardiovascular system by increasing heart rate and improving cardiac output will also be carefully examined. The assumption is that the changes in blood pressure (systolic/diastolic) have a decisive impact on the metabolism of drugs, including vasopressors/inotropics, which in turn affects their choice and fluid therapy.6.There will be no follow-up period.7.•date and time of birth•birth weight•gestational age•type of delivery•pH and BE and pCO2 from umbilical cord blood, or blood from the first hour of life•sex•Apgar score 1–5–10 min.The following information will be recorded for each echocardiogram:•Examination date•Internal temperature of the neonate in °C•fraction of inhaled oxygen (FiO2)•perfusion•systolic/diastolic/mean arterial pressure•diuresis, hematocrit, creatinineThe following data will be recorded:•the need for catecholamines, type of drug, dose or other key drugs: anticonvulsants, nitric oxide (NO), surfactant•the need for mechanical ventilation (including in the first 72 h of life)•the need to implement continuous positive airway pressure (CPAP) support within 3 days of life•occurrence of pneumonia•occurrence of periventricular bleeding, type of cerebral injury (ultrasound and magnetic resonance imaging (MRI)•patient's death•length of hospital stayThe study will use an electronic database.Baseline data will be collected from the hospital electronic database. The following patient data will be collected:Entries and corrections to the electronic database will be made solely by the researcher on an ongoing basis. In order to verify the compliance of the data stored in the electronic database with the original source data, access to the source documentation  will be accessible to the bioethics committee and regulatory authorities. Responsibility for compliance will rest with the principal investigator. The electronic database will conform to the original source data. Periodic checks will be carried out for possible errors and inconsistencies in the data entered.8.Complete patient and examination information will be stored on a secure, password-protected platform. Only researchers participating in the study will receive a personalized login and password to access information from the study. The statistical team will not have access to confidential data. All relevant medical history data, including copies of ultrasound clips and radiological reports, will be stored separately in electric or paper form in closed folders.9.H0 when it is in fact false. The strength and error rate of Type II depend on the specific value of the alternative defined in H1. The power depends directly and primarily on the following factors:•the size of the sample used in the study•the actual size of the effect, i.e., the expected alternative hypothesis•the adopted significance levelTo calculate the power for the F test in a design with one factor having k levels we will define the hypotheses,iμ signifies the mean for level and factor.Analysis of sample power and size optimises the use of resources in the study design, increasing the chances of obtaining conclusive results with maximum efficiency. The power is 1 minus the type II error value, i.e., the probability of rejecting F test for equality of means in the model (H0). The F-statistic distribution in the case of the null hypothesis is the central F distribution, while in the alternative hypothesis it is the non-centralized F distribution with the decentrality parameter λ. Therefore, power can be defined as the probability that the F-statistic follows the decentralized distribution. The exact power is calculated as:The power calculation is based on the 10.The research is observational and non-interventional. Echocardiography and ultrasound examination of the cerebral and renal circulation is an essential diagnostic tool in neonates treated with TH and will not otherwise disrupt the diagnostic and therapeutic process of the neonate. Biological material—will not be collected for the purposes of the study.11.Neither the parents of the patients nor the general public will be involved in developing the questions, measuring outcomes, or developing the study design. There are no plans to involve patients in the recruitment and conduct of the study.12.The effect of TH and the warming phase on the cardiovascular system, including cerebral, visceral and renal circulation will be determined. The intention is to attempt to show the impact of each phase on the metabolism of drugs, including vasopressor/inotropic drugs, which in turn affects the choice and fluid therapy.13.The Bioethical Committee of the Medical University of Warsaw has approved the study (KB 55/2021). All significant modifications to the protocol will be reported to the committee. Written informed consent will be obtained from all parents/caretakers of infants who are willing to participate in the study. The consent for participation in the study can be withdrawn at any time, without consequences and without an obligation to justify the decision. All deidentified data collected during the trial will be available. These documents will be accessible to anyone who provides a methodologically sound proposal immediately following publication with no end date. We plan to submit our findings to international peer reviewed journals and conferences .14.Asphyxia (A) is characterized by hypoxia and hypercapnia, which occur due to lack of oxygen or ischemia. However, when it lasts longer it can have primarily deleterious effects on the brain, in addition to being associated with impaired organ perfusion, and can result in multiple organ failure.It also seems likely that hypoxic-ischemic encephalopathy (HIE) is secondary to multi-organ dysfunction, primarily cardiopulmonary failure after asphyxia, and is not solely caused by hypoxia , 17. BecThe number of cardiovascular failures in neonates with asphyxia ranges from 25% to 60% , 21 to 7The direct impact of TH on the cardiovascular system includes moderate bradycardia, increased pulmonary vascular resistance (PVR), inferior filling of the left ventricle (LV) and LV stroke volume , 22. TheIn light of the above written question, and given that one of the goals of therapeutic whole-body hypothermia is to suppress metabolism, is the change we observed simply an adaptive response?The effect of TH and the warming phase on the cardiovascular values has a decisive impact on the metabolism of drugs, including vasopressors/inotropics, which in turn affects the choice of medication and fluid therapy. Thus, our attention should be shifted from the brain to other organs that may impair the nervous system.New therapeutic targets must be directed toward normalizing circulation and counteracting the consequences of cardiovascular damage in HIE.


The intricate interplay between cardiovascular (CV) pathology and chronic kidney disease (CKD) encompasses diagnostic protocols , outcome assessments , as well as advancements in new therapeutic approaches . This bidirectional relationship is highly complex. Recent advancements in biomarkers, echocardiographic diagnostic techniques, contrast-free coronary angioplasty procedures, and novel renal denervation methods have opened avenues for modulating outcomes previously unexplored. These breakthroughs hold promise for preserving renal function and enabling the early identification of subclinical CV damage in patients with advanced renal conditions.Journal of Clinical Medicine aimed to present the diverse CV implications associated with acute and chronic renal diseases while exploring different facets of diagnosis and the latest advancements in therapeutic strategies. As the coordinators of this issue, we view it as highly significant and captivating, setting the stage for future endeavors such as Issue 2.0 and other forthcoming projects. Its solid impact and potential pave the way for continued exploration and innovation in the field.This Special Issue from the The contributors of the seven articles featured in this issue comprise a mix of cardiologists, including clinicians, sonographers, intensivists, interventionists, and nephrologists with expertise in chronic dialysis and renal transplantation. This issue encompasses three articles based on substantial patient cohorts, a narrative review, a meta-analysis, and two additional systematic reviews.In the setting of CKD, the increased risk of CV mortality cannot be entirely attributed to conventional CV risk factors alone, suggesting a multifactorial etiology. One influential factor implicated in this process is the presence of uraemic toxins, which can impact the structure and function of the arterial system and potentially contribute to the development of CV diseases. In a comprehensive literature review, Foudi et al.  describeA retrospective analysis of a single-center registry database with ESKD patients in chronic hemodialysis who underwent percutaneous coronary interventions (PCIs) explored the debatable cardiovascular benefits of statins during a 10-year follow-up period . The autProlonged uremia in advanced CKD can lead to subclinical cardiac fibrotic damage. Evaluating myocardial strain using echocardiographic techniques allows for detecting functional changes in the heart muscle within the context of advanced CKD. In addition, specific fibrosis biomarkers such as procollagen type I carboxy-terminal propeptide (PICP), procollagen type III N-terminal peptide P3NP), and galectin-3  can be measured to assess paraclinical signs of myocardial fibrosis. The study of Ureche et al. [NP, and gIn the meta-analysis published in this section, Brinza et al.  evaluateArterial hypertension is a global public health issue, with resistant hypertension presenting a higher risk of cardiovascular events. In a systematic review, Burlacu et al. explored the potential of arterial stiffness as a predictor of response to renal denervation (RDN) in patients with resistant hypertension . Ten stuThe most recent guidelines from the European Society of Cardiology (ESC) have highlighted notable and highly reliable recommendations  regarding reducing iodinated contrast agent usage in PCIs for patients with severe CKD. These recommendations aim to prevent the further deterioration of renal function and subsequent mortality increase. Additionally, these guidelines strongly advocate for using low- or iso-osmolar contrast media at the lowest feasible volume in this specific patient population. In this context, Burlacu and colleagues systematically evaluated the existing evidence on the safety and efficacy of minimum- or zero-contrast intravascular ultrasound (IVUS)-guided PCIs in patients with CKD . The resFurthermore, the use of IVUS guidance allowed for better visualization of the coronary anatomy and improved procedural success rates. Based on these findings, IVUS-guided PCI could be a safe and effective alternative to conventional PCI in CKD patients . However, further studies are needed to confirm these results and to identify specific patient populations or clinical scenarios where this approach may be particularly beneficial.Given the current context of the SARS-CoV-2 virus pandemic, Genovesi and colleagues published in our section the results of a multicenter study on patients hospitalized with COVID-19 . A cohorIn conclusion, this issue, despite its heterogeneous nature and specialized focus, showcases the immense potential of research in the field of cardio-nephrology in enhancing diagnostic methods, prognostic assessment, complication risk evaluation, and the utilization of novel therapeutic approaches for patients with advanced kidney disease and associated cardiovascular complications. It highlights the significant advancements being made to improve patient care and outcomes in this unique patient population.


Atrial fibrillation (AF) is prevalent, especially in patients with heart failure. Their prevalence increases with age and both conditions are interrelated. Electrocardioversion (ECV) is considered a safe and effective procedure and is among one of the recommended therapies to terminate AF back to normal sinus rhythm. Our study highlights one of the rare complications following ECV.A 71-year-old female with a history of atrial fibrillation underwent electrocardioversion and developed sudden onset of ventricular stunning resulting in refractory cardiogenic shock. She was treated with mechanical cardiac support including IABP and Impella. Both provided minimal support then rapid clinical deterioration happened leading to imminent death.Patients with atrial fibrillation and heart failure treated with electrocardioversion might develop refractory cardiogenic shock and death as a complication of this procedure.The online version contains supplementary material available at 10.1186/s12872-023-03376-8. AF has been more prevalent in the United States given the growth of the older population. In 2010, around 5.2 million patients had AF and it was estimated to reach up to 12.1 million by 2030 . InteresA 71-year-old female with a history of AF on anticoagulation complicated by tachycardia-induced cardiomyopathy and systolic HF (baseline EF of 45%) presented to the emergency due to a sudden onset of dyspnea and palpitations. Her vital signs were initially stable with BP = 112/64 and HR = 150. On physical examination, she had jugular venous distension, irregular heart rhythm with a rate of 150bmp, and reduced air entry bilaterally with crackles at the bases of the lung. Also, she had bilateral pitting edema.2), with normal mass (LV mass index = 83.3 g/m2), with mildly reduced systolic function EF = 45%. There is mild global hypokinesis of the left ventricle. The mitral valve leaflets appear thickened, but open well, with no valvular stenosis, but moderate amount of mitral regurgitation. By PISA method, the effective regurgitant orifice area (ERO) is 0.19 cm [She has a history of diabetes mellitus, hypertension, hyperlipidemia, rheumatic fever as a child, moderate mitral regurgitation without stenosis, AF, and HF with reduced EF. She was diagnosed with AF in 2014 and was placed on metoprolol and Rivaroxaban. 2 months prior to her current hospitalization, she underwent cardioversion which temporarily terminated AF. A month later, patient elected to undergo catheter ablation instead being placed on antiarrhythmics, therefore, she had catheter ablation for a recurrent AF which was able to revert her heart rhythm back to NSR. Her ambulatory transesophageal echocardiogram showed: The left ventricular cavity size is normal  with a QTc of 410 msec , we attempted a dose of 5 mg IV metoprolol without any response, then 150 mg bolus of IV Amiodarone followed by an amiodarone infusion (1 mg/min) for 8 h and it was not successful in improving her HR with worsening of her symptoms. Therefore, an urgent cardioversion was planned . A quick pre-interventional bedside TTE revealed presence of a small pericardial effusion without tamponade activity, global mild left ventricular hypokinesis with mildly reduced systolic function (EF = 40–45%) and ruled out right ventricular dysfunction. A synchronized ECV at 200 J was performed and was successful in restoring NSR , Figs. To our knowledge, this is the first study to report a case with AF complicated by AIC that was treated with ECV and developed immediate refractory cardiogenic shock unresponsive to mechanical cardiac support including IABP and Impella.Atrial fibrillation has been associated with an increased risk for heart failure incidence and presence of both condition leads to worse prognosis . EvidencA study on 119 cases showed that ECV is a safe and effective procedure to be performed in the ED as no life-threatening arrhythmias or peripheral thromboembolism were recorded . Almost Our patient had a prior history of rheumatic fever as a child and refractory atrial fibrillation that was unresponsive to pharmacological cardioversion, catheter ablation and even ECV. Given her acute presentation, her AF was likely complicated with AIC leading to a cumulative burden on her heart, making her susceptible to abrupt deterioration with a ECV. Based on her echocardiographic findings following ECV, myocardial stunning was highly suspected. Cardiac stunning has been defined as a prolonged mechanical myocardial dysfunction impairing ventricular or/and atrial activity which might occur due to different factors including postischemic ventricular dysfunction, vascular/endothelial injury, postischemic metabolic dysfunction or long-lasting impairment of neurotransmission with alterations in the heart electrophysiology . In our Refractory cardiogenic shock due to ventricular stunning is a very rare complication after electrocardioversion and further research to identify patients at risk for this fatal complication is warranted.Sudden ventricular stunning one of the rare but possible complication following electrocardioversion in patients with AF leading to death.Early identification and prompt treatment of such a complication might improve the outcomes.Below is the link to the electronic supplementary material.Supplemental video 1: Parasternal long axis echocardiogram showing diffuse reduction in the wall motion of the left ventricle with an EF of 20%. Percutaneous heart pump is placed in the left ventricle passing the aortic valve