The effect of hypothyroidism on the cardiovascular system has been well documented. Cardiac dysfunction due to hypothyroidism manifests as both systolic and diastolic dysfunction of the heart leading to cardiac arrhythmia and congestive heart failure. Its presentation in the form of refractory hypotension is rare. We describe a 52 year old man on whom Hypothyroid Cardiomyopathy manifested as cardiogenic shock responsive only to thyroxin replacement. A 52 year old man with nausea and vomiting of two days duration was found to be hypotensive and in acute hypoxic respiratory failure requiring mechanical ventilation. The patient is known to have hypothyroidism and he has been non compliant with oral Synthroid therapy. Hypotension persisted in spite of aggressive initial fluid resuscitation. The electrolytes, renal function, white blood count and hemoglobin were all within normal limits. Blood TSH level was 69.45 mU/L (0.35-5.50 mU/L); T4 level was 0.454 ng/dl (0.93-1.7 ng/dL) and T3 level was 29.87 ng/dl (84-202 ng/dL) all indicative of severe primary hypothyroidism. The Chest x-ray revealed normal heart size with pulmonary congestion. The EKG revealed a heart rate of 96/min with normal axis and rhythm and without ischemic changes. Patient remained hypotensive in spite of initiation of dopamine infusion. A bed side echocardiography revealed a left ventricular ejection fraction (LVEF) of 30% with global hypokinesia. The isovolumetric contraction time and isovolumetric relaxation time were prolonged with increased myocardial performance index (MPI) of (0.56) indicating that there was both systolic and diastolic dysfunction. An echocardiogram done six month ago showed a normal LVEF and normal MPI.Hypotension persisted in spite of high dose dopamine infusion. In the absence of evidence of myocardial ischemia hypothyroidism was considered to be responsible for the observed acute refractory hypotension/cardiogenic shock. Intravenous thyroxin at a dose of 0.050 mg was administered and the dose increased to 0.075 mg in the next 48 hours resulting in stabilization of the blood pressure and weaning off the dopamine and subsequently weaned off ventilator during the next 72 hours. A repeat echocardiography done in one month revealed normal LV function with LVEF of 60% with normal MPI of 0.35.The effects of thyroid hormone on cardiac function are well documented . ThyroidHypothyroid cardiomyopathy can manifest as cardiogenic shock and only thyroxin replacement can restore hemodynamic stability by reversing the systolic and diastolic dysfunction.(LVEF): left ventricular ejection fraction; (MPI): myocardial performance index.A written informed consent was obtained from the patient for publication of this case report. A copy of the written consent will be made available on request.The above mentioned authors declare that they have no competing interests.DS, OB, SJ treated the patent and were responsible for writing the paper and looking up the background references. RV, PK was responsible for over all coordination and final proof reading. All the above mentioned authors read and approved the final manuscript.


Bedside emergency ultrasound has rapidly developed over the past several years and has now become part of the standard of care for several applications. While it has only recently been applied to critically ill pediatric patients, several of the well-established adult indications may be applied to pediatric patients. One of the most important and life-saving applications is bedside echocardiography. While bedside emergency ultrasonography does not serve to replace formal comprehensive studies, it serves as an extension of the physical examination. It is especially useful as a rapid and effective tool in the diagnosis of pericardial effusions, tamponade and in distinguishing potentially reversible causes of pulseless electrical activity from asystole. Most recently, left ventricular function and inferior vena cava measurements have proven helpful in the assessment of undifferentiated hypotension and shock in adults and children. Future research remains to be carried out in determining the efficacy of bedside ultrasonography in pediatric-specific pathology such as congenital heart disease. This article serves as a comprehensive review of the adult literature and a review of the recent applications in the pediatric emergency department. It also highlights the techniques of bedside ultrasonography with examples of normal and pathologic images. The field of Pediatric Emergency Medicine is a relatively new field of medicine developed in the 1980s. The mereUltrasound technology was originally introduced in the 1950s and portable scanners made their way into the adult emergency department in the 1980s.4 The firThe use of bedside ultrasound is only beginning to emerge in the field of Pediatric Emergency Medicine and has not yet been formally incorporated into the subspecialty fellowship curricula. While numerous applications for pediatric patients are being realized, there is a strong desire for pediatric-specific training. Thus farOne such life-saving application for bedside or point-of-care ultrasonography is echocardiography. Echocardiography is the gold standard for the diagnosis of cardiac and pericardial abnormalities and is a non-invasive modality for detecting life-threatening cardiac conditions. The incorporation of bedside echocardiography has been shown to have a significant impact on medical decision-making and is a useful adjunct to the clinical exam when radiologic and laboratory studies are often unreliable and non-specific.13 A receThus far, well-established indications for bedside emergent echocardiography in adult populations include the evaluation of blunt and penetrating chest trauma and critically ill patients. Emergency physicians may rapidly and effectively assess the presence of pericardial effusion, tamponade, cardiac activity, global assessment of contractility and the detection central volume status. In patie7To date, there is a paucity of research dedicated toward the application of bedside echocardiography in pediatric patients. Potential extensions of adult applications to pediatric populations include evaluation for the presence of a pericardial effusion and in cardiac arrest (asystole and PEA). Additional applications may include the assessment of global wall motion and function and the assessment of undifferentiated hypotension.24et al. studied bedside ECHO performed by emergency physicians in patients at a high risk for pericardial effusions, revealing an overall accuracy of 98%, sensitivity of 96% and specificity of 98%.[One of the earliest and most well-recognized applications for bedside echocardiography is for the identification of pericardial effusions in traumatic and non-traumatic conditions. It is especially crucial to promptly identify pericardial effusions and tamponade as these may lead to life-saving interventions. Mandavia y of 98%. Pericardy of 98%. On sonoget al. reported a 100% sensitivity, 99% specificity and 99% overall accuracy for the identification of pericardial effusions in patients with chest trauma.[et al. showed that bedside ECHO improved the outcome of patients with penetrating chest trauma with shorter time to diagnosis (15.5 vs. 42.4 min) and better overall survival (100% vs. 57%).[et al. highlighted the importance of the ability to identify pericardial effusion and early signs of tamponade in facilitating surgical management of patients with cardiac rupture secondary to blunt non-penetrating chest trauma.[In trauma patients, Ma t trauma. In a 10-vs. 57%). In a cast trauma. These ret trauma.30Of particular clinical importance is the development of tamponade, which may lead to cardiovascular collapse and, ultimately, death. Cardiac tamponade is defined as significant compression of the heart by accumulating pericardial contents and fluid. While asEchocardiography is the most sensitive and specific means of detecting tamponade and has st attempt and a 1% major complication and a 3% minor complication rate.[The treatment of tamponade includes emergent pericardiocentesis or drainage of the pericardial fluid. “Few medical situations exist in which a simple, quickly performed medical procedure can result in immediate life-saving results.” The roution rate.Approximately 16,000 American children suffer out-of-hospital cardiac arrest per year . When compared with adults, children are more likely to survive arrest, with greater than 10% of the children surviving to hospital discharge. Among those treated for in-hospital cardiac arrest, 2/3 can be successfully resuscitated with return of spontaneous circulation and greater than 25% survive to hospital discharge. Overall,Pulseless cardiac arrest is the cessation of cardiac activity and the absence of palpable central pulses. In children, it is especially important to determine whether a pulse is present to initiate early basic and advanced life support to improve survival. Unfortunet al. and Salen et al. showed that no patients with sonographic cardiac standstill had ROSC, regardless of the initial presenting rhythm.[It is difficult to predict survival outcomes from pulseless cardiac arrest. Pediatric resuscitations may be for extended periods of time, often devoting considerable resources. Bedside echocardiography has the potential to give us more information that may ultimately allow us to predict survival outcomes, and terminate resuscitative efforts in futile situations. In a study of adult patients with out-of-hospital cardiac arrest, no patients who required greater than two doses of epinephrine or who had greater than 20 min of resuscitation without Return of spontaneous circulation (ROSC) survived. Blaivas g rhythm.48 Converg rhythm. It has bg rhythm.50A common presenting problem in the emergency department is dehydration. This is especially common in pediatrics, with approximately 9% of the children presenting diagnoses. Unfortunet al. reported that with limited focused training, emergency physicians can assess the left ventricular (LV) jection fraction accurately.[The sonographic assessment of left ventricular function or ejection fraction may be useful in patients presenting with unexplained hypotension or shock. This may expeditiously narrow the differential diagnosis  to begin early aggressive and appropriate resuscitation. Bedside curately.et al. studied the IVC diameter in relation to a 450 mL blood donation. Results suggested that IVC measurements could be a reliable indicator of even small amounts of blood loss.[56Another means by which ultrasound can aid in evaluating shock and hydration status is the estimation of CVP by performing measurements of the IVC. Echocardiograph measurement of the IVC was first introduced as an estimation of right-sided cardiac function and was ood loss. However,ood loss.5657 Durid loss.56 With dehd loss.56et al. showed that this ratio was lower in clinically dehydrated children and that it increased with the administration of IV fluid boluses.[In a recent study, dehydrated children were compared with normally hydrated pediatric patients presenting to the emergency department. The maximum and minimum IVC diameter measurements were lower and there was greater collapse in clinically dehydrated patients, suggesting that a collapsed IVC may reliably predict dehydration. However, boluses. This evaet al. presented the bedside limited echocardiography by emergency physicians, which combined a protocol of LV function estimation and IVC measurement to apply to the assessment of a pediatric patient presenting with undifferentiated hypotension or shock. When over-read by pediatric cardiologists, the emergency physicians were able to obtain acceptable quality images and accurately assess the left ventricular function and IVC volume.[The UHP ultrasound protocol utilized the three sonographic applications of identifying free fluid, qualitative cardiac assessment and abdominal aorta as part of the evaluation of an adult patient in PEA or with undifferentiated hypotension. In pediaC volume.The incidence of congenital heart disease in the United States is approximately 8-10 cases per 1,000 live births. The age at presentation can vary according to the specific type of lesion. Further, while cardiac emergencies are uncommon in children and the majority of children do not present with ischemic heart disease, the majority of cardiac pathology encompasses congenital heart disease. Such anatomic lesions include tetralogy of Fallot, hypoplastic left heart, atrial septal defects (ASDs) and ventricular septal defects (VSDs) to name just a few. While the identification of particular congenital heart lesions is complex and beyond the scope of bedside echocardiography, patients may present with associated pathology that immediately affects cardiac care.et al. highlighted cases of cardiac disease masquerading as acute bronchospasm. Further cardiac presentations include adolescents who may be evaluated for “sentinel events” and are at risk for sudden cardiac death. Other pathologies include infective endocarditis, hypoxemic attacks  and acute rheumatic fever.[Of particular concern is the infant who presents with shock and it is difficult to distinguish between primary respiratory pathology and congenital heart disease associated with ductal closure. Pershad ic fever. Bedside ic fever. There reLow-frequency transducers should be used for the cardiac assessment with a 2–5 MHz curvilinear probe with a small footprint to allow for imaging between the ribs . While tWhen approaching a pediatric patient, in particular, positioning and patient comfort is paramount. Smaller children often require more preparation and patience. Measures to improve patient comfort and compliance with examinations include warmed gel, laying in the parents lap and pacifiers or feeding during the examination. Because children have much smaller and superficial structures than adult patients, it is important to adjust the depth of the images accordingly.Standard views for bedside echocardiography include subxiphoid, parasternal long-axis, parasternal short-axis and apical 4-chamber views. Angling and tilting of the transducer may be necessary to obtain images. It is important to note that all abnormal findings should be confirmed with several views.21 AdditiThe subxiphoid view is the preferred view in the FAST examination and it is most useful during resuscitation as it does not typically interfere with resuscitation procedures. The probe marker should be oriented to the patient’s right side and should be placed subcostally, just below the xiphoid process, directing the probe in the direction of the patient’s left shoulder. The probe itself is quite flat and should be held at a 15-degree angle to the patient’s body, in contrast to most other positionings that are perpendicular to the patient’s body .The subxiphoid view utilizes the liver as an acoustic window and readily visualizes all four chambers of the heart . It is mrd and 4th intercostal space, above the level of the nipple line. The probe marker should be directed toward the patient’s left hip or in 4:00 direction [The parasternal long-axis view is the preferred view for the assessment of left ventricular contractility and for the identification of pericardial effusions when adequate subxiphoid images cannot be obtained. The probe is placed perpendicular to the chest wall, immediately to the left of the sternum, between the 3irection . A distiirection .et al. reported that visual estimation of cardiac function into normal mild, moderate or severe dysfunction is as good or better than other more complex, calculated methods.[The parasternal long-axis view is best utilized to measure contractility. In the review of methods of sonographically determining LV function, McGowan  methods. The left methods.The parasternal short-axis view readily evaluates the contractility and valvular function. Once the parasternal long-axis view is obtained, the transducer should be rotated 90 degrees in order to obtain the parasternal short-axis view. The probe marker should be directed toward the patient’s right hip or in the 6:00 direction . One canth intercostal space, just lateral to the nipple. The probe marker is typically oriented toward the patient’s right side [The apical 4-chamber view is the preferred view for evaluating the relative dimensions of the right and left sides of the heart. The transducer is placed at the cardiac apex, which may be located by palpating the point of maximal impulse (PMI). This is typically located at the T4-T5 level, at the 5ght side . The patght side . An examght side .2, which collapses by 50% during quiet inspiration.[The transducer is placed in the subxiphoid position  and the piration. Absolutepiration. In adultpiration.. One canpiration.. A propopiration.M-mode, or motion mode, allows for a one-dimensional tracing of structure movement over time. In the parasternal long-axis view, the cursor may be placed over the walls of the left ventricle in order to assess for contractility . This isTamponade is the indication for pericardiocentesis . The parWhile bedside ultrasound has only recently been incorporated into the practice of Pediatric Emergency Medicine, several well-established adult applications may be applied toward the care of pediatric patients. Most notable are the identification of pericardial effusions and tamponade, the assessment of PEA and asystole, global contractility and IVC evaluation for hydration status. More research remains to be performed with the application of bedside ultrasonography with regards to the early recognition of congenital heart disease and for other pediatric-specific pathologies.


It has been suggested that, in late gadolinium enhancement, the signal of right ventricular myocardium is nulled at a shorter inversion time than the left. While we initially made the same observation, we believe that the difference is not real, but results from artifacts.We present 7 cases as well as computer simulations to describe the nature of these artifacts and explain how they can create the impression of different inversion times for the right and left ventricle. At inversion times that are shorter than ideal for the myocardium a black rim can be seen at the border of the myocardium with blood on the inside and with fat on the outside. This is most likely a partial volume effect. The thin myocardium of the right ventricle is sandwiched between these black rims and, at a low spatial resolution, is no longer visible. In this case, the adjacent black rims may then be misinterpreted as myocardium. While black rims also occur on the left side, the myocardium is thicker and remains discernable as a separate layer. As a consequence, the optimal inversion time for the right ventricle only appears different from that for the left. In fact, in the presence of hypertrophy of the right ventricle or during systolic wall thickening we did not find a difference in inversion times between the left and right ventricle. We conclude that sufficient spatial resolution is important for adequate late gadolinium enhancement of the right ventricle. Late Gadolinium Enhancement (LGE) sequences have become a routine part of cardiovascular magnetic resonance (CMR) for ischemic heart disease, myocarditis and the cardiomyopathies -6. In pei, General Electric Medical Systems, Milwaukee, MI, USA) using a 4-channel surface coil and a spoiled gradient refocused echo sequence, without phase sensitive reconstruction (PSIR) capabilities. The settings were as follows: Field of view (FOV) 34 – 40 cm, matrix 256 × 192, slice thickness 7.0–8.0 mm, minimum echo (TE) and repetition (TR) times , flip angle 20°, bandwidth 31.25 kHz, number of excitations  2, views (lines) per segment (VPS) 24, trigger delay set to target diastole.All LGE sequences followed 10 to 20 minutes after a bolus of 0.2 mmol/kg of dimeglumine gadopentetate . Cases 1–4 were performed on a 1.5 Tesla scanner , using a 12-channel cardiac coil and a double inversion steady state free precession sequence (IR TrueFisp), with the following settings: In-plane resolution 1.5 mm by 3 mm for patient 5, 1.5 by 1.1 mm in diastole and 2.1 by 1.5 in systole for patient 6, 1.6 by 1.6 mm as well as 2.6 × 2.6 mm for patient 7 and 1.4 × 1.4 mm for patient 8, slice thickness 7 mm for patients 5 and 6, 10 mm for patient 7 and 7 as well as 10 mm for patient 8, TE 1.02 to 1.34 ms, TR 8.2 to 9.0 ms, NEX 2, VPS 65. In order to obtain the systolic image in patients 5 and 6 the data were acquired every three heart beats instead of every two in order to target systole early after the R spike. The temporal resolution was shortened to target a period of minimal cardiac motion at the end of systole by reducing the VPS to 40. TI was chosen to produce a black rim artefact in patient 5.Assuming T1 times for gadolinium-containing blood, myocardium, and fat of 330 ms, 450 ms, and 300 ms, respectively, we generated a computer model of a ventricle in short axis with simulations of these three tissues from the inside to the outside. The virtual ventricle is surrounded by zero signal, mimicking the air-filled lungs. The simulations included varying TIs and in-plane resolutions.Case 1  from that for the myocardium. At the optimal TI for myocardium, the endocardium may be difficult to discern because both the signal of the endocardium and that of blood would be greater than zero. The thin grey endocardium between the black myocardium and the grey blood may not form a strong enough contrast with the latter.Although the presented case examples act as reasonably strong evidence for the concept of similar TIs in the RV and LV myocardium it would be further proven by a systematic study acquiring and comparing higher and lower resolution datasets. It would be expected that the high resolution data would show agreement in the LV and RV null times, while the lower resolution data would show an apparent difference. An animal study could also compare the true thickness of the RV myocardium with what is measured in LGE imaging at different TIs. Clinical trials in patients with pathology of the RV anterior free wall are indicated to assess the usefulness of systolic LGE imaging.This study only relates to magnitude reconstructed late gadolinium enhanced imaging and not the phase sensitive inversion recovery (PSIR) approach that is now increasing being used. The use of (PSIR) leads to a display that is rather insensitive to TI and does not have a dark rim artefact as described . AlthougFrom our observations, we deduct that the TI for the RV is similar to that of the LV. Black rims at the interfaces between endocardium and cavity and between epicardium and epicardial fat with a thin and hardly discernable layer of myocardium in between may be misinterpreted as nulled RV myocardium. This may falsely suggest a TI that is different from optimal for the LV myocardium. In clinical practice, it may be advisable to choose the TI slightly too long rather than too short to avoid the black rim artifact that obscures RV myocardium. In-plane spatial resolution should not be lower than 1.5 mm in order to account for the thin RV free wall. Imaging in systole rather than diastole may present a superior strategy when targeting subtle and diffuse areas of LGE in the RV free wall.LGW carried out part of the clinical studies, participated in its design and coordination, and drafted the manuscript. CM participated in the design and conceptualization of the physical background of the black rim artifact. LV carried out the computer simulations. SJY conceived of the study, participated in its design and coordination and supervised the clinical studies. All authors read and approved the final manuscript.


Myocardial contrast echocardiography (MCE) is a relatively simple myocardial perfusion imaging technique which should be used in different clinical settings. The ability of MCE to provide a comprehensive assessment of cardiac structure, function, and perfusion is likely to make it the technique of choice for non-invasive cardiac imaging.Contrast agents are encapsulated microbubbles (MB) filled with either air or high-molecular-weight gas. They are innocuous, biologically inert and when administered intravasculary, the sound backscatter from the blood poll is enhanced because MB have the enormous reflective ability due to a large acoustic impedance mismatch between the bubble gas and surrounding blood.MCE is an ideal imaging tool for the assessment of left heart contrast and the myocardial microcirculation. MCE detects contrast MB at the capillary level within the myocardium and, thus, has the potential to assess tissue viability and the duration of the contrast effect. MCE was equivalent to SPECT for the detection of CAD with a tendency toward higher sensitivity of MCE compared with SPECT in microvascular disease and CAD. MCE is also a bedside technique that can be used early in patients presenting with acute heart failure to rapidly assess LV function  and perfusion (rest and stress). The MB are smaller than the capillaries and should flow freely through the coronary circulation. It is important to remember that the actual risk associated with contrast is very small, especially if physician follow the contrast administration recommendations that suggest avoiding the use of MB in unstable and critically acute ill patients.Contrast agents are encapsulated microbubbles (MB) filled with either air or highmolecular-weight gas. They are innocuous, biologically inert and when administered intravasculary, the sound backscatter from the blood poll is enhanced (non-linear acoustic behaviour) because MB have the enormous reflective ability due to a large acoustic impedence mismatch between the bubble gas contenent and surrounding blood.The ability of MB to produce strong backscattered acoustic signal is based on their compressibility, which depends on the viscoelastic and pressure properties of the shell and gas. MB encapsulation is required to increase stability and persistence, which depends on rigidity and provides persistence and good resistance to blood pressure changes and US pressure waves. A degree of fragility is needed to allow the destruction and posterior myocardial refilling. Another approaches to extend MB survival are the use of gas with low solubility and diffusibility.1). The signal intensity depends on MB concentration: at low concentration the signal intensity increase linearly; as the concentration increases, the relationship between MB and signal intensity becomes curvilinear until it reach a plateau, where the contrast effect may actually decrease.The diameter of MB is one of the major determinants of scattering behavior because the scattering cross section is extremely dependent on the bubble size and is directly proportional to the sixth power of its radious . Larger The interaction between MB and US produces compression during pressure peaks and expansion during pressure nadirs. It appears a remarkable and fortuitous coincidence that gas bubbles of a size required to cross the pulmonary capillary vascular resonate in a frequency range of 1.5–7 MHz, precisely that used in diagnostic US echocardiography. The oscillation of MB may produce a wide range of harmonic frequencies: subharmonic , 3, seco® or by adherence to microparticles (Levovist)®. Replacing air with a low solubility fluorocarbon gas stabilises bubbles still further ®, greatly increasing the duration of the contrast effect. Third generation agents—not yet commercially available—will use polymer shell and low solubility gas and should produce much more reproducible acoustic properties. These properties allow passage of the pulmonary vasculature, opacification of the left ventricular cavity, and imaging of myocardial perfusion. Currently, the most used second-generation contrast agents are Sonovue® , Optison® , and Definity®  (Table 1). These agents differ in terms of their shell constituents and gas content that influence shell-stiffness and stability of the MB, and determine physical properties [The first agents capable of left heart contrast after intravenous injection (first generation agents) were air bubbles stabilised by encapsulation (Albunex)operties . Even ifMyocardial contrast echocardiography (MCE) is an ideal imaging tool for the assessment of the myocardial microcirculation. MCE detects contrast MB at the capillary level within the myocardium and, thus, has the potential to assess tissue viability. At baseline, approximately 8% of left ventricular mass is constituted by blood present in the microcirculation termed myocardial blood volume (MBV), 90% of which is comprised of blood in the capillaries. In normally perfused myocardium, the rate of capillary blood flow is 1 mm/s. Saturation of the coronary microvasculature by MB therefore takes about 5 s (because the thickness of the US beam is approximately 5 mm). When there is no flow limiting stenosis, MBF increases 5 times during hyperemia (stress testing), and therefore the myocardium replenishes in 1 s. In addition, a flow-limiting stenosis leads to a reduction in capillary blood volume in the distal microvasculature, with an accompanying decrease in signal intensity during MCE. These 2 features (slowed contrast appearance and decreased capillary blood volume) form the basis for detecting CAD using MCE. However, because the US beam used to detect the MB also destroys them at normal power outputs, the lower the MBF the longer the time required to achieve peak video intensity.2).The mechanism of US images enhancement depends on MB’behavior under acoustic pressure. The enormous reflective ability of MB is due to a large acoustic impedence mismatch between the bubble gas content and the surrounding blood. In contrast to MB, cardiac tissue produces much fewer harmonic frequencies, so selective reception of harmonic echos will preferentially detect signals emanating from contrast agent rather than the myocardium. Although these methods improved the signal-to-noise ratio, off-line image processing is frequently required to evaluate myocardial perfusion, because tissue signals is still present. Harmonic imaging also used high acoustic powers that destroyed MB consequently, the imaging frame rate had to be reduced substantially with electrocardiographic triggering to allow MB to replenish the myocardial microcirculation between pulses (Table 1). to distinguish nonlinear MB signals from tissue. Reflected echos are scaled and subtracted. Because tissue responds linearly , subtraction and scaling results in zero signal. MB reflect nonlinearly, so received echos will not be canceled out, enabling selective MB detection. Most of these multipulse techniques additionally use power Doppler, and the resulting signal is color coded and displayed. Because high-power imaging destroys MB, imaging of myocardial perfusion cannot be performed in real time. Low MI imaging increases signal-to-noise ratio and because of minimal MB destruction continuous imaging may be performed. Both high- and low-power MCE have their advantages and disadvantages. High-power imaging precludes continuous imaging owing to destruction of contrast, and therefore wall motion cannot be assessed simultaneously. On the other hand, signal-to-noise ratio is good. Low-power imaging allows simultaneous assessment of perfusion and contraction but has a lower sensitivity for the detection of MB.These include high-power modalities with superior tissue noise suppression that allow on-line assessment of myocardial perfusion and low-power modalities that permit imaging with high frame rates. These modalities specifically take advantage of the nonlinear behavior of MB in an acoustic field. Many techniques use multiple transmitted pulses that are, e.g. full and half amplitude  would preclude most applications in the intensive care unit/critical care unit. Likewise the recommendation that patients be monitored for 0.5 h after injection will limit use in portable studies on nonmonitored hospitalized patients and, in many laboratories will complicate outpatient studies. This would only require extension of the postprocedure monitoring [MB can potentially affect the heart by mechanical obstruction of the coronary vessels or cause direct cell damage when destroyed in high-intensity sound fields. Mechanical obstruction can occur when bubbles larger than capillary diameter are injected into the coronary circulation. However, the bubbles are generally smaller than the capillaries and should flow freely through the coronary circulation. Even without a specific mechanism, the fatal aderse events in unstable patients suggest that increased caution is appropriate. First, it is important to remember that the actual risk associated with contrast is very small. Second, the new list of contraindications for encapsulated MB contrast agents  are regulated by changes in MBV , relative US intensity ratios within different myocardial regions reflect relative ratios of both MBV and MBF in these regions. It is well known that in the presence of a stenosis, MBF remains constant until the stenosis is severe . MBF is maintained by vasodilation and/or recruitment of <300-μm microvessels distal to the stenosis. Thus, it is accepted that at rest, MBV increases within the bed supplied by a stenotic artery. Because it causes vasodilation of all microvessels, it is also generally assumed that MBV is equal between beds supplied by stenosed and nonstenosed vessels during exogenous hyperemia. Since during exogenous hyperemia, MBV and flow are closely coupled, the ratios of video intensities from different beds have been demonstrated to reflect the ratios of MBF to those beds.4). All 3 agents have been widely used for pharmacologic stress-TESTS [Stress agent. The most commonly used stress agents are adenosine, dipyridamole, and dobutamine  is based on the triad of clinical history, electrocardiography, and laboratory investigation. These methods, although useful, can often be nondiagnostic in this setting. Because MCE is the only technique that permits immediate assessment of wall motion and perfusion, it has a unique role in the diagnosis of ACS . Myocardet al.  were theet al. . Besideset al. . The preet al.  was the et al. . Converset al. . Patientet al. , 26.The ability of MCE to predict functional recovery is comparable to that of cardiovascular magnetic resonance imaging . Thus thet al. [The study by Aggeli et al.  demonstrAn exercise test is the most widely used technique for the assessment of CAD, but it has a relatively low sensitivity and specificity compared with imaging techniques such as stress echocardiography and SPECT imaging.et al. MCE was equivalent to SPECT for the detection of CAD with a tendency toward higher sensitivity of MCE compared with SPECT. The latter is likely because MCE, by virtue of its superior spatial resolution compared with SPECT, is likely to identify mild subendocardial ischemia due to CAD more effectively.Stress echocardiography is excellent for the assessment of CAD, but its sensitivity tends to be compromised in patients with significant left ventricular hypertrophy (LVH). Perfusion techniques like SPECT may suffer from low specificity, because hypertensive patients may have microvascular disease in the absence of large vessel CAD and often asymetrical LVH, which result in a relative difference in tracer uptake leading to apparent perfusion abnormalities even in the absence of microvascular disease and CAD. The MCE in this scenario is an ideal technique . PerfusiMCE is a bedside technique that can be used early in patients presenting with acute heart failure (AHF) to rapidly assess LV function  and perfusion (rest and stress) . DemonstMyocardial contrast echocardiography is a relatively simple technique for imaging of myocardial perfusion that should be used in different clinical settings. The ability of MCE to provide a comprehensive assessment of cardiac structure, function, and perfusion is likely to make it the technique of choice for non-invasive cardiac imaging. MCE is accurate in distinguishing different patterns of myocardial perfusion suggesting a potential risk-stratification technique in subjects without a prior history of CAD or clinical features suggestive of an ACS.


General techniques1.1. Stress and safety equipment1.2. Left ventricular (LV) structure and function module1.3. Right ventricular (RV) structure and function module1.4. Gadolinium dosing module.1.5. First pass perfusion1.6. Late gadolinium enhancement (LGE)2. Disease specific protocols2.1. Ischemic heart disease2.1.1. Acute myocardial infarction (MI)2.1.2. Chronic ischemic heart disease and viability2.1.3. Dobutamine stress2.1.4. Adenosine stress perfusion2.2. Angiography:2.2.1. Peripheral magnetic resonance angiography (MRA)2.2.2. Thoracic MRA2.2.3. Anomalous coronary arteries2.2.4. Pulmonary vein evaluation2.3. Other2.3.1. Non-ischemic cardiomyopathy2.3.2. Arrhythmogenic right ventricular cardiomyopathy (ARVC)2.3.3. Congenital heart disease2.3.4. Valvular heart disease2.3.5. Pericardial disease2.3.6. Masses Monitoring equipment 2. Preparation and regular practice for rapid removal of the patient from the magnet3. Emergency resuscitation policy in place4. Defibrillator5. Drugs for emergency treatmenta. Immediately at hand: β-blocker (eg esmolol or metoprolol), nitroglycerin, aminophyllineb. In the emergency cart: full set of emergency drugs 6. For dobutamine – on-line assessment of wall motion during image reconstruction performed immediately after image acquisitionDobutamine typical maximum dose of 40 ug/kg/minAtropine 0.25 mg fractions typical Adenosine 140 μg/kg body weight/min• Severe systemic arterial hypertension (≥ 220/120 mmHg)• Unstable angina pectoris2)• Significant aortic valve stenosis  block• 2• Sinus bradycardia (heart rate < 45 bpm)• Systemic arterial hypotension (< 90 mmHg)• Narrow-angle glaucoma• Myasthenia gravis• Obstructive uropathy• Obstructive gastrointestinal disorders1. Obtain informed consent for the stress test2. To fully exert its effects patients should refrain from the following medications for at least 24 hours prior to the examination due to potential of counteraction against stress agent:Dobutamine: β-blockers and nitratesAdenosine: caffeine , theophylline, dipyridamole3. Fasting is not usually considered mandatory, but is sometimes advised because recognized adverse effects of stress drugs include nausea and vomiting, which is problematic when lying supine in the restricted space of the magnetDobutamine at high doses may cause chest pain, palpitations. More severe complications are uncommon, including:• infarction• ventricular fibrillation• sustained ventricular tachycardiaAdenosine may cause flushing, chest pain, palpitations, breathlessness. More severe side effects include• transient heart block• transient hypotension• transient sinus tachycardia• bronchospasm1. Scout imaging – transtransaxial, coronal, sagittal2. Transaxial (8–10 mm) set of steady state free precession (SSFP) or fast spin echo images through the chest.3. Scout to line up short axis images – cine acquisitions are preferable to single shot as long axis motion and inflow should be visualizeda. Vertical long axis prescribed orthogonal to transaxial scouts aligned through the apex and center of the mitral valveb. Horizontal long axis aligned orthogonal to the vertical long axis, passing through the apex and center of the mitral valve4. Steady state free precession short axis cine images, from the mitral valve plane through the apex. The basal most short axis slice should be located immediately on the myocardial side of the atrioventricular junction at end-diastole prescribed from the previously acquired long axis cines.a. Slice thickness 6–8 mm, with 2–4 mm interslice gaps to equal 10 mm.b. Temporal resolution ≤ 45 ms between phasesc. Parallel imaging used as available5. Steady state free precession long axis cine imagesa. The 4 chamber long axis is prescribed from the vertical long axis through the apex and center of the mitral and tricuspid valves. This can be cross-checked on basal short axis cines, using the costophrenic angle (margin) of the RV free wall.b. Vertical long axis, prescribed from the scout already acquiredc. LV outflow tract (LVOT) long axis, passing through the apex, the center of the mitral valve and aligned with the center of LVOT to aortic valve, as seen on a basal short axis cine.d. Optional – a set of more than 3 rotational long axis views can be obtained.6. Analysisa. All short axis images are evaluated with computer-aided analysis packages for planimetry of endocardial and epicardial borders at end-diastole and end-systole. More advanced software automatically adjusts for systolic atrioventricular ring descent.b. The inclusion or exclusion of papillary muscles in the LV mass should be the same as that used in normal reference ranges used for comparison.c. Care must be used at the 1 or 2 most basal slices. Due to systolic movement of the base towards the apex in normally contractile ventricles, the end-systolic phase will include only left atrium. This may not be the case in a severely dysfunctional LV. Either way, this slice at end-diastole will include LV mass and volume.1. Right ventricular (RV) short axis views can be obtained in a similar fashion to the LV structure and function module. If the short axis is used for quantification, it is important to place the basal short axis slice immediately on the myocardial side of the right ventricle and to take extra care to exclude appropriate amounts of atrial volume from at least one basal slice at end systole.2. Transaxial stack of cines covering the RV enable best identification of the tricuspid valve plane.3. Long axis images should include an RV vertical long axis view aligned with tricuspid inflow and a RV outflow tract view .4. Analysisa. A similar computer-aided analytic approach is required as for the left ventricle.b. Care must be taken with RV trabeculations and with the RV outflow tract after repair of tetralogy of Fallot with a consistent approach used for longitudinal comparison.Notes:1. Volumes and injection rates depend on scan duration: the given values are recommendations for typical scan times.2. Injection rates are different for 1 molar contrast agents. As a general rule, divide the given injection rates by a factor of 2.3. Contrast agents with higher relaxivity  require smaller doses.4. Throughout the protocols, the term "gadolinium" refers to gadolinium chelates5. Injection rate for peripheral angiography with elliptic-centric readouts may be different than those specified below.See Table 1. Scout imaging as per LV structure and function module2. Saturation-recovery imaging with gradient echo-echo planar (GRE-EPI) hybrid, GRE, or SSFP readout3. Short-axis view imaging (at least 3 slices per heart beat)a. For ischemia evaluation, must obtain data every heart beatb. Slice thickness 8 mmc. Parallel imaging, 2-fold acceleration, if availabled. In-plane resolution, ~< 3 mme. Readout temporal resolution ~100 – 125 ms or shorter as availablef. Contrast is given  followed by at least 30 ml saline flush (3–7 ml/sec)g. Breathhold starts during early phases of contrast infusion before contrast reaches the LV cavity.h. Image for 40–50 heart beats by which time contrast has passed through the LV myocardium1. Need at least 10 minute wait after gadolinium injection (0.1–0.2 mmol/kg). Note – The delay may be shorter than 10 minutes if lower doses are used as blood pool signal falls below that of late enhanced myocardium.2. 2D segmented inversion recovery GRE imaging during diastolic stand-still3. Same views as for cine imaging (short- and long-axis views)4. Slice thickness, same as for cine imaging5. In-plane resolution, ~1.4–1.8 mm6. Acquisition duration per R-R interval below 200 ms but should be less in the setting of tachycardia.7. Inversion time set to null normal myocardium. Alternative is to use fixed TI with a phase-sensitive sequence.8. Read-out is usually every other heart beat but should be modified to every heart beat in the setting of bradycardia, and every third heart beat in the setting of tachycardia or arrhythmia.9. Optionala. Single-shot imaging (SSFP readout) performed as backup for patients with irregular heart beat, difficulty breath holding.b. 3D sequences with parallel imaging in appropriate patients if signal-to-noise is sufficient.10. Analysisa. Interpret visually using AHA 17-segment model.b. Estimate area  of enhancement within each segment .1. LV structure and function module2. Optional – T2 weighted imaging (see nonischemic cardiomyopathies protocol for sequence details) 3. First pass perfusion module (only at rest)4. To look for microvascular obstruction, scan for consider repeat first pass perfusion sequence or early gadolinium enhancement, i.e within the first 1–3 minutes after contrast infusion5. Late gadolinium enhancement module1. LV structure and function module2. Optional – low dose dobutamine with 5–10 minute infusion of 10 μg/kg/min of dobutamine to assess contractile reserve as improvement in wall thickening3. Optional – adenosine stress-rest perfusion or high dose dobutamine functional imaging (see stress protocols for more details) to determine the presence of inducible perfusion deficits or wall motion abnormalities4. Late Gadolinium Enhancement module5. Analysisa. Helpful to view cines and LGE images of equivalent planes side-by-sideb. Interpret using both cine and LGE data. For example, "region is dysfunctional but viable".1. LV structure and function module2. Dobutamine stimulationa. Increase the dobutamine in increments of 10 μg/kg body weight/minute every 3 minutes starting at 10 μg/kg body weight/minute until target heart rate [85% × (220-age)] reached.b. Add atropine in small incremental doses, if heart rate response is poor.c. Repeat 3 short axis and 3 long axis cine views during each incrementd. Continuous ECG monitoring and BP measured during each stage.e. View cine loops online as they are being acquired.f. Adapt the SSFP cine sequence to optimize temporal resolution as needed as the heart rate increases.g. Stop test for new wall motion abnormality, serious side effect, or achievement of peak heart rate.3. Analysisa. View cines in multiscreen format, reviewing rest, intermediate stress levels and peak stress at the same time in a synchronized fashion.b. Describe wall motion as normokinetic, mild hypokinetic, severe hypokinetic, akinetic and dyskinetic for all 17 segments.c. Report inducible wall motion abnormalities and viability.1. LV structure and function module 2. Two intravenous lines should be available, one for gadolinium and one for adenosine, one in each arm. Preferential site of contrast infusion is antecubital. Blood pressure cuff should be used with care taken not to interfere with gadolinium or adenosine infusion.3. Adenosine stress perfusion imaging (at least 3 minute infusion of 140 ug/kg body weight/min). Option – initial adenosine infusion may be performed with the patient outside the bore of the magnet.a. First pass perfusion moduleb. During last minute of adenosine, gadolinium is injectedc. After imaging for 40–50 heart beats by which time gadolinium has passed through the LV myocardium, adenosine is stopped.d. Continous ECG monitoring and BP measured at baseline, during infusion, and for at least 2 minutes post-infusion of adenosine.4. Rest Perfusiona. Need at least 10 minute wait for gadolinium to wash out from stress perfusion imaging. During this period stress images can be reviewed, cine imaging can be completed (e.g long-axis views), valvular evaluation can be performed, etc.b. Perfusion imaging repeated without adenosine using same dose of gadoliniumc. If stress images are normal and free of artifacts, rest perfusion can be skipped. Additional gadolinium may be given as needed for late gadolinium enhancement 5. Late Gadolinium Enhancement modulea. Need to wait at least 5 minutes after rest perfusion6. Analysisa. Interpret visually using 17 segment AHA segment model b. Optional – Quantitative analysis of the inflow curves could be considered in cases without obvious visual perfusion defect.c. Helpful to view cines, stress and rest perfusion, and LGE images all side-by-side in equivalent slices1. Peripheral vascular coil, or combination of coils, as available. Venous compression cuffs  are helpful, if available.2. Transaxial, low-resolution, vessel scouting with time-of-flight MRA or SSFP.3. Gadolinium timinga. Option 1 -Transaxial test bolus at level of distal abdominal aorta. 2 ml injection of gadolinium, followed by 20 ml saline. Determine time to peak enhancement following injection using a single-shot bolus tracking sequence.b. Option 2 – Bolus trigger technique to time start of scan4. Stepping-table, gadolinium-enhanced MRA performed in the coronal projection from the mid abdominal aorta to the feet.a. Two volumetric acquisitions – one pre-contrast (for subtraction) and one during contrast administration.b. Gadolinium injected in 2 phases to minimize venous contamination followed by saline bolus.c. Slice thickness 1–1.5 mm; acquired spatial resolution in-plane 0.8–1.5 mm.d. Slices – typically 60–80, as needed to accommodate vessels of interest.e. Volumes obtained of abdomen/pelvis and thighs may be coarser spatial resolution (larger vessels), while those of the legs preferably are sub-millimeter spatial resolution. The former acquisitions typically require 15–20 seconds, while the leg acquisition may take 60–90 seconds for increased spatial resolution. Elliptical centric k-space acquisition is advantageous for the legs. If available, time-resolved acquisitions are preferred for the legs.f. Parallel acquisition recommended (multichannel surface coil needed)5. Analysisa. 3D reconstructions may be helpful for an initial overview and visualizing the vasculature tree, but generally should not be used for primary decision making.b. Primary diagnoses are made by scrolling through source images , and using selected thin slab MIP and MPR reconstructions in optimized orthogonal and oblique views for each station. The presence, number, and degree of stenoses are evaluated qualitatively.Alternative: dual injection protocol1. Single dose of gadolinium: time-resolved MRA of the calf and foot vessels2. Single dose of gadolinium: abdominal and thigh vessels1. Localizer, 3 orientations2. Half-fourier single shot fast spin echo or SSFP Transaxial orientation.3. Transaxial T1-weighted fast spin echo through aorta 4. SSFP cine imaging in parasagittal plane parallel to aorta Option – use 3-point piloting5. Evaluate aortic valve as per valvular protocol6. Contrast timinga. Option 1 -Transaxial test bolus at level of distal abdominal aorta. 2 ml injection of gadolinium, followed by 20 ml saline. Determine time to peak enhancement following injection.b. Option 2 – Bolus triggering technique to time start of scanc. Option 3 – Rapid multiphase 3D acquisitions without timing7. 3D gadolinium enhanced MRA (0.1–0.2 mmol/kg) a. Use spatial resolution of at least 1–1.5 mm b. Parallel acquisition if availablec. At least 2 acquisitions after contrast injection8. Optional – transaxial T2-weighted gradient echo or T1-weighted gradient-echo post-contrast for aortitis9. Analysis – MPR-Reconstruction, MIP and thin slab MIP1. LV structure and function module to look for wall motion abnormalitiesa. Add repeat horizontal long axis with high temporal resolution sequence (≤ 20 ms per phase) to accurately determine quiescent period of RCA2. Navigator-gated, 3D, free-breathing, MRA sequence:a. Transaxial slices spanning from level of proximal main pulmonary artery down to the middle of the right atrium (entire cardiac coverage if desired). Slice thickness 1–1.5 mm; acquired spatial resolution in-plane of 1.0 mm or less.b. Slices – typically 50–80, as needed to encompass vessels of interest.c. Adjust trigger delay and acquisition window according to observed quiescent coronary period.d. Parallel acquisition preferrede. Navigator placed over the right hemi-diaphragm.f. Optional – contrast to increase vessel conspicuity3. Optional -a. breathhold techniques if poor image quality or navigators unavailable or of poor qualityb. T2-prepared sequence may be useful1. LV structure and function module2. Breathhold non-gated contrast-enhanced MRA performed in the coronal projection encompassing the pulmonary veins and left atrium (greater anterior coverage if breathholding permits) a. Gadolinium (0.1–0.2 mmol/kg) injected at 2–3 ml/sb. Slice thickness 1–2 mm; acquired spatial resolution in-plane 1–1.5 mm.c. Slices – typically 60–80, as needed to encompass region of interest.d. Parallel acquisition used as availablee. 2–3 volumetric acquisitions – each breathhold typically no longer than 15–18s.3. Optional – through plane phase contrast flow analysis through each pulmonary vein.4. AnalysisGadolinium MRA evaluated qualitatively by scrolling through slices in various orientations. The number and position of pulmonary veins is accounted for noting common trunks, accessory veins, and evidence for stenosis or thrombosis. A 3D workstation is used for MPR analysis to calculate major and minor axes, and cross sectional area of each pulmonary vein ostium. Compare pre- and post-ablation images side by side. 3D rendering may facilitate planning of surgical or electrophysiologic interventions.1. LV structure and function module2. Consider T2-weighted imaging in the acute setting when necrosis/edema may be present (e.g. myocarditis)a. Body coil should be used or alternatively functional surface coil intensity correction algorithmsb. Breath-hold, segmented fast spin-echo imaging (double inversion recovery)c. Perform imaging prior to contrast administrationd. Selected slices based on cine imaging findings (e.g. 2 and 4-chamber long axis and 3 representative short axis slices)e. Adjust readout to mid-diastolef. Slice thickness at least 10 mmg. Slice thickness of dark blood prep if used should be greater than the base-apex motion of the mitral annulus3. Late Gadolinium Enhancement modulea. Analysis – Examine the "pattern" of enhancement as certain nonischemic cardiomyopathies have predilection for scarring in typical ways4. Optional – adenosine stress-rest perfusion imaging or high dose dobutamine stress functional imaging (see stress protocols) to comment on the presence or absence of ischemia since a mixed cardiomyopathy may be present5. For hypertrophic cardiomyopathies -LV outflow tract flow imaging for presence of turbulence, systolic anterior motion, and phase velocity measures of gradient if present.1. LV structure and function module – consider 5–6 mm slice thicknessa. Careful RV as well as LV volumetric analysis.2. Transaxial or oblique transaxial SSFP cine images covering the RV including RVOT. An RV vertical long axis view aligned with tricuspid inflow is recommended.3. Optional sequencesa. Selected transaxial or oblique transaxial black blood images (double inversion recovery T1-weighted fast spin echo).b. Repeat same geometry with fat suppressionc. Late gadolinium enhancement module in same orientations as above. Consider T1 nulling for RV.d. Consider use of anterior surface coil only to improve resolution without "wrap around" artifacts.e. Consider prone position in overweight patients in order to minimize distance between the surface coil and RV.Major criteria for diagnosing ARVC include severe dilation and reduction of right ventricular ejection fraction with no or mild left ventricular involvement; localized right ventricular aneurysms (akinetic or dyskinetic areas with diastolic bulgings); severe segmental dilation of right ventricle. Minor criteria include mild global right ventricular dilation or ejection fraction reduction with normal left ventricle; mild segmental dilation of right ventricle; regional right ventricular hypokinesia. All of these are demonstrable by CMR as performed above. CMR also allows assessment of fatty infiltration and myocardial fibrosis. However, the latter two findings are not part of current guidelines.Note – there is variability of the structure and shape of the RV amongst normals, so there is a tendency for inexperienced observers to overdiagnose RV wall motion abnormalities. For example, relative end-systolic bulging of a thin but contractile region of the RV free wall adjacent to the moderator band can be a normal finding and basal short axis cines may give the impression of inferior wall dyskinesis due to normal through-plane motion. Careful study of RV cines in volunteers and a range of patients is recommended before attempting identification of ARVC.For all diagnoses:1. LV and RV structure and function modulea. In many cases, a contiguous stack of transaxial SSFP cine images from the inferior wall of the LV through the top of the aortic arch is recommended.b. Gradient echo cine or hybrid gradient echo/echo planar imaging may be added for improved detection of turbulent flow in particular planes2. Scout imaging in the plane of the ascending aorta and main pulmonary artery.3. Through plane velocity encoded cine imaging through the main pulmonary artery and aorta to measure Qp and Qs.4. Time resolved or multiple rapid dynamic 3D gadolinium enhanced magnetic resonance angiography in a coronal orientationFor individual diagnoses, protocols must be individualized. Additional sequences to consider:1. For shunt lesionsa. Measurement of Qp:Qs as aboveb. In plane and/or through plane velocity encoded gradient echo sequence to visualize rather than measure shunt flow2. For lesions involving the great vesselsa. SSFP cine imaging in parasagittal plane parallel to aortab. Specific alignment of cines with jet flow through aortic coaractation, flowed by through-plane jet velocity mapping to measure peak velocity and recognize possible diagnostic prolongation of forward flowc. Assessment of valves as per valvular protocold. SSFP cine and/or gradient echo cine images along the individual pulmonary arteriese. Comparison of RPA with LPA flow volume in the case of unilateral branch PA stenosis.Patients with artificial valves can safely undergo CMR at 1.5 and 3 Tesla. The force exerted by the beating heart is many-fold higher than the force exerted by the magnetic field.1. LV structure and function module.a. Use horizontal long axis to look for valve anatomy and turbulence of the mitral and tricuspid valve.b. Use LVOT view for mitral and aortic valve.c. Use vertical long axis for mitral valve.d. Coronal view for aortic valvee. Additional views .2. Specifica. Valve morphology assessment with SSFP cine in the plane of the valve in question. Care must be taken to optimize the level and angle of imagingb. Note – if planimetry of a stenotic valve is to be attempted, a contiguous or slightly overlapping stack of high resolution cines transecting the line of the jet and moving from orifice level to immediately downstream is recommended. Planimetry is most likely to be valid where the cross section of the orifice, or rather of the jet, is clearly delineated. This may not always be the case due to fragmented or oblique jet flow.c. Gradient echo or hybrid gradient echo/echo planar imaging may visualize regurgitant jets with a higher sensitivity .d. In mitral or tricuspid regurgitation, a contiguous stack of 5 mm cines is recommended aligned with the direction of inflow and transecting the principal line of coaptation, moving from the more superior commissure to the inferior. The orientation can be that of the LVOT plane for the mitral and transaxial for the tricuspid. Such a stack enables assessment of tethering, prolapse, or regurgitation through the scallops of both mitral leafletes.3. Measure flow velocity and volume perpendicular to the vessel distal to valve leaflet tips.a. Adapt velocity encoding to actual velocity .b. Use lowest TE possible for high velocity jet flows.c. The CMR software should routinely correct for phase errors due to concomitant gradients. As long as this is the case, background phase errors due to eddy currents may be correctable by normalizing velocities to reference in static tissue.4. Analysis:a. Determine left and right ventricular stroke volume using volumetric analyses of SSFP cine sequences to measure single valve regurgitation.b. Mitral regurgitation can be measured by subtracting aortic flow from the LV stroke volume.c. Multiple valve lesions can be assessed from comparison of the aortic and pulmonary diastolic regurgitant flow and the LV and RV stroke volumes.d. Measure aortic valve area by direct planimetrye. Alternatively, measure aortic valve area by  × Area LVOTf. Calculate peak mitral valve gradient from peak mitral valve flow1. LV structure and function module2. T1 or T2-weighted fast spin echo imagesa. 2–3 representative long axis images and 3–4 representative short axis images to measure pericardial thickness b. If pericardial cyst is suspected, refer to masses protocol3. Optional – If regions of thickened pericardium noted – T1-weighted gradient echo myocardial tagged cine sequences to demonstrate presence or absence of epicardial/pericardial slippage (2–3 long axis images and 1–2 short axis images)4. Optional, but encouraged if available – real-time imaging in the short axis during dynamic breathing maneuvers for evaluation of ventricular interdependence5. Late Gadolinium Enhancement module1. LV structure and function module2. T1 weighted fast spin echo – slices through the mass and surrounding structures (number of slices depends on size of the mass)3. T2 weighted fast spin echo with fat suppression  – through the mass and surrounding structures as above. See nonischemic cardiomyopathies for sequence details.4. First pass perfusion module with slices through mass5. Repeat T1 weighted turbo spin echo with fat suppression6.  Repeat selected steady state free precession cine images post-contrast7. Late gadolinium enhancement module – note that TI to null the mass may be different than for myocardium.CMK wrote protocols, edited protocols, edited manuscript, corresponding author, JB wrote protocols, edited protocols, edited manuscript, SDF wrote protocols, edited protocols, edited manuscript, RJK wrote protocols, edited protocols, edited manuscript, EN wrote protocols, edited protocols, edited manuscript. All authors read and approved the final manuscript.


Congenital heart block is a rare complication of pregnancy associated with Sjögren Syndrome that may result in the death of the foetus or infant, or the need for pacing in the newborn or at a later stage.The case is presented of a 64-year-old patient with primary Sjögren Syndrome and a history of having given birth to two sons with congenital heart block, both of whom required pacing several years later.The literature relating to this association is discussed including the suggested mechanism, long-term outcome of mothers of children with congenital heart block and preventive treatment strategies. As it primarily affects the lachrymal and salivary glands, the chief clinical features are dry eyes and a dry mouth [Sjögren Syndrome is an autoimmune disease of exocrine glands that occurs with a prevalence of 0.5 – 1% [ry mouth .Congenital heart block occurs in a frequency of 1 in 20,000 live births. It has been reported to occur in 2% of Ro-positive mothers ; 5% of m9 (reference range: 1.3–3.5 × 109), a raised ESR of 38 (reference range: 1–15) and a raised CRP of 8 mg/L (reference range:0–4 mg/L). She was anti-Ro and anti-La positive and IgG levels were raised at 26.2 (5.3–16.5 g/L). Her whole flow rate was 0 ml/min and the parotid flow rate was markedly low at <0.1 ml/min. C. albicans counts were raised. Her management was based on maintaining good hydration. The superimposed candidal infection was treated by 1-week courses of Nystatin 100,000 IU/ml oral suspension, repeated every 4 weeks.A 64-year-old Caucasian lady with Sjögren Syndrome was referred to the Oral Medicine department from Rheumatology. She complained of dry mouth, eyes and vagina; intermittent swelling of the salivary glands and aching joints. She was diagnosed with primary Sjögren Syndrome 35 years earlier. At presentation, her management regime consisted of 5 mg prednisolone, Oral Balance Gel, sugar-free chewing gum and Viscotears. Her other medications were lansoprazole 15 mg, hydroxychloroquine 200 mg and thyroxine 75 mcg daily. She was a retired journalist. She did not smoke. She drank 14 units of alcohol a week, mainly red wine. She was married with 5 sons; 2 of whom had congenital heart block. The first son was 41 years old and had required no treatment. The second son was 25 years old and had required a pacemarker at age 4 years and later required a heart transplant at 13 due to cardiomyopathy. Extraoral examination revealed mild skin bruising. Intraorally, the mucosa was dry with no salivary pooling and no milkable saliva from the major gland orifices. Blood investigations revealed lymphopenia at 0.9 × 10An association between congenital heart block (CHB) and connective tissue diseases such as lupus and Sjögren Syndrome has been reported in the literature . There iA study by Buyon et al examined 105 mothers with Ro and/or La positive sera, and reported that 113 infants were diagnosed with CHB. Of the 87 pregnancies with adequate records, bradyarrhythmias detected before 30 weeks gestation in 71 (82%) – median 23 weeks. Of the 113 infants, 22 (19%) died, mostly within 3 months of birth. Of the 107 live-born children, 67 (63%) required pacing; 35 within 9 days, 15 within 1 year and 17 after 1 year. Of the 49 mothers who had subsequent pregnancies, 8 (16%) had another child with CHB [The underlying mechanism behind congenital heart block in Sjögren Syndrome is suggested to be due to Ro and La antigens present on apoptotic blebs on surface of actively remodelling foetal cardiocytes. Opsonized Ro & La antibodies can then lead to macrophage activation, TNF-α & TGF-β secretion which favours differentiation of fibroblasts into collagen-secreting myofibroblasts which promote scarring . The sitIt is thought that foetal CHB arises due to increased susceptibility of the foetal heart due to increased apoptotic remodelling of foetal heart cells or lower density of L-type calcium channels. Other antibodies such as muscarinic type-1 receptor (M1R) antibodies described in maternal blood may also have a role. Foetal heart expresses M1R while maternal heart expresses mainly M2R. The majority of cases of CHB are subclinical at birth; with a case reported of normal ECG at birth and subsequent development of asymptomatic heart block at 2 years .Discordance for CHB has been reported in monozygotic twins despite identical genetics and environmental exposure to maternal anti-Ro antibody . Late-onet al studied the long-term outcome of 64 children with complete heart block, and found that 60% (32 out of 53) of the mothers tested were anti-Ro and/or anti-La positive. The mean follow-up period was 121 months, and the mean maternal age was 38. At the time of delivery, the majority of mothers (66%) were healthy [It is recommended that infants with CHB require close follow up, not only of cardiac rate & rhythm, but also of ventricular function. Press in utero, continuing after birth to monitor rate, rhythm and ventricular function [Potentially serious outcomes are rare but possible, with 63% of affected offspring requiring pacing. The general recommendation is to monitor foetal cardiac function from 16–24 weeks function .The optimal treatment is still debatable but corticosteroids may be of benefit in established cases and may further have a role in the prevention of congenital heart block in mothers with previously affected pregnancy. Thus, treatment of congenital heart block is based on fluorinated steroids that cross the placenta. The use of glucocorticoid intervention for 3–19 weeks in cases of foetal second degree heart block may increase the likelihood of reverting to first degree heart block rather than progression to third degree heart block . DexametThe evidence to support prophylactic treatment to prevent congenital heart block during subsequent pregnancies is weak, and concerns regarding the safety of fluorinated steroids have been raised, particularly neurological toxicity, spontaneous abortion, stillbirths & intrauterine growth restriction. Other interventions, such as intravenous immunoglobulins, plasmapeheresis and azathioprine have been suggested .In summary, congenital heart block is a common occurrence in offspring of mothers affected with Sjögren Syndrome. Whilst there is no consensus on management, appropriate referral and follow-up is recommended. Finally, a diagnosis of Sjögren Syndrome should be considered in a mother who has a child diagnosed with congenital heart block.Written informed consent was obtained from the patient as per the standard protocol at Guy's Hospital NHS Foundation Trust.The authors declare that they have no competing interests.All authors were involved in patient diagnosis and management, with PJS and MPE being the senior clinicians guiding overall management at the time. KAM wrote the manuscript under the general guidance and supervision of TWJP.K.A.M., BDS, MFDRCSI, MSc is currently a Clinical Research Training Fellow at the University of Southampton. Prior to that, he had been a postgraduate student and research fellow at Guy's Hospital (the study site). He is a member of the British Society for Oral Medicine, British Society for Oral and Maxillofacial Pathology, International Association for Oral Pathology and the International Association for Dental Research. He has won numerous clinical and research prizes including the Royal Society of Medicine's President's Prize of the Odontology Section  and the British Society for Oral Medicine's clinical and research papers prize (2009).P.J.S., BDS, LDSRCS, FDSRCS, is a Consultant in Oral Medicine and the Clinical Director for Dental Services at Guy's Hospital, London (UK).M.E.P. BDS, MBBS, FDSRCS, MRCP, FDSRCS(OM), MD is a Senior Lecturer and Honorary Consultant in Oral Medicine at Guy's Hospital (UK).T.W.J.P. BDS, MBBS, FDSRCS, MRCP, FDSRCS(OM) is currently a Consultant in Oral Medicine at King's College Hospital, London. He has trained in both dentistry and medicine and at the time of the study was a Specialist Registrar and Honorary Lecturer in Oral Medicine.


Cardiac resynchronization Therapy (CRT) is an effective therapy for chronic heart failure with beneficial hemodynamic effects leading to a reduction of morbidity and mortality. The responder rates, however, are low. There are various and contentious echocardiographic parameters of myocardial asynchrony. Patient selection by echocardiographic assessment of asynchrony is thought to improve responder rates.In this small single-center pilot-study, seven established parameters of myocardial asynchrony were used to select patients for CRT: (1) interventricular electromechanical delay , (2) Septal-to-posterior wall motion delay , (3) maximal difference in time-to-peak velocities between any two of twelve LV segments (Ts-12 ≥ 104 ms), (4) standard deviation of time to peak myocardial velocities , (5) difference between the septal and basal time-to-peak velocity , (6) left ventricular electromechanical delay  and (7) delayed longitudinal contraction .16 chronic heart failure patients  at least two out of seven parameters of myocardial asynchrony received cardiac resynchronization therapy (CRT-ICD). Follow-up echo examination was after 6 months. The control group was a historic group of CRT patients (n = 38) who had not been screened for echocardiographic signs of myocardial asynchrony prior to device implantation.Based on reverse remodeling , the responder rate to CRT was 81.2% in patients selected for CRT according to our protocol as compared to 47.4% in the control group (p = 0.04). At baseline, there were on average 4.1 ± 1.6 positive parameters of asynchrony . Only the LVEMD decreased significantly after CRT (p = 0.027). The remaining parameters showed a non-significant trend towards reduction of myocardial asynchrony.The implementation of different markers of asynchrony in the selection process for CRT improves the hemodynamic response rate to CRT. Cardiac resynchronization Therapy (CRT) is an effective therapy for chronic heart failure with beneficial hemodynamic effects and a reduction of morbidity and mortality -7. DespiIn the CARE-HF study  with an Accounting for the complexity of the parameters of asynchrony and the lack of a clear predictor, the indications for CRT in the current guidelines do not include echo parameters of myocardial asynchrony  and an eThere is no diagnostic gold standard to determine myocardial asynchrony. Echocardiography is considered as an objective tool to evaluate myocardial intra- and interventricular asynchrony. However, when assessing myocardial asynchrony, some parameters cannot be reliably measured in all patients. Integrating multiple parameters might therefore improve the diagnostic sensitivity and specificity of asynchrony tests in the individual patient.The goal of this pilot study was to improve the response rate to CRT by prospective patient selection by echocardiography.This is a prospective single center study evaluating the improvement of CRT response by implementing a new echocardiographic approach in patient selection for CRT-ICD.Inclusion criteria were: chronic heart failure in the functional classes NYHA III-IV with a LVEF < 0.35, QRS > 120 ms and at least two positive echo parameters of myocardial asynchrony (combination of two intraventricular or combination of one inter- and one intraventricular parameter). Patients with more than two myocardial segments of akinesia (suggesting scar tissue) or left ventricular aneurysms (end-diastolic thinning of the myocardium < 5 mm) were excluded from this study.In order to obtain unbiased data regarding cardiac improvement, standard and individually optimized heart failure medication  remained unchanged 3 months prior to implantation of CRT in all patients. Follow-up was performed after 6 months.The historic control group (n = 38) comprised patients from our hospital that had received CRT in recent years. The inclusion criteria for these patients were identical: NYHA III-IV with a LVEF < 0.35 and a QRS width > 120 ms. All patients received a CRT- ICD and were fully documented by 2D and Tissue Doppler echocardiography at baseline. The CRT patients underwent 6 months follow-up examination, including echocardiography.The AV-interval was set individually in all patients according to . There wEchocardiography was performed on a Vivid 7 . The images were stored digitally and analyzed off-line by EchoPac PC Dimension . For TDI and 2D echocardiography analysis, three beats were stored.Seven parameters of intra- and interventricular asynchrony were used [see table The interventricular electromechanical delay (IMD) is the time difference between the left ventricular and right ventricular electromechanical delays . The cut-off value for interventricular asynchrony is > 40 ms , additio.The septal-to posterior wall motion delay (SPWMD) is obtained from M-mode in the parasternal long axis as the shortest interval between the maximal contraction of the septum and the maximal contraction of the left posterior wall. The cut-off value for interventricular asynchrony is ≥ 130 ms ,15, addi, addi15,The maximal difference in time-to-peak velocities between any two of twelve LV segments (Ts-12) and the standard deviation of time-to-peak myocardial velocity (Ts-12-SD) are assessed with Tissue Synchronization Imaging (TSI). 12 myocardial segments in the apical views  are analyzed. These parameters with a cut-off value ≥ 34.4 ms (Ts-12-SD) and ≥ 104 ms (Ts-12) were previously prescribed as powerful predictors of response to CRT [, additioThe difference between the basal septal and basal lateral Ts is assessed with TDI in the apical four chamber view by color-coded TDI (TDId). The cut-off value ≥ 60 ms is a predictor of successful CRT , additio.The left ventricular electromechanical delay (LVEMD) or aortic pre-ejection delay is measured as the time between the onsets of the QRS to aortic flow. The cut-off value of this parameter is > 140 ms indicating intraventricular asynchrony , additio.The delayed longitudinal contraction (DLC) is assessed with tissue tracking in the apical four chamber, two chamber and long-axis views for the detection of LV segments with mechanical asynchrony. The highest possible frame rate was chosen according to , additio. We consAccording to previous studies, we defined successful resynchronization therapy as a relative reduction of the LV end-systolic volume of more than 15% and a relative increase of the LVEF of more than 25% compared to baseline -21. The Written consent was obtained from each patient, and the ethics committee of the Charité University Hospital approved the protocol.2-test. The level of significance was p ≤ 0.05.Statistics were calculated using SPSS . Results are expressed as mean (± standard deviation). Comparisons of non-parametric variables between the "echo-guided CRT" patients and the control group were calculated by Wilcoxon test. The comparison of echocardiographic parameters between groups was calculated by unpaired Whitney-Mann test. Dichotomized data were analyzed by the Chi16 patients with more than two positive echocardiographic parameters of asynchrony received an ICD-CRT ("echo-guided CRT" group).The historic controls (n = 38) were chosen because of the complete echocardiographic follow-up at 6 months after CRT. The controls did not differ in regard to their baseline data: age, baseline QRS width and LVEF. However, there were more female patients in the control group (p = 0.04). Table The echo-guided CRT-group had 4.1 ± 1.6 positive parameters of asynchrony at baseline Table . After 6There was a clinical improvement in the echo-guided CRT group . The responder rate in the "echo-guided CRT" group was 81.2% compared to 47.4% in the control group (p = 0.04). The reverse remodeling after CRT was significant in both groups  to predict CRT benefit is presented as area-under-the-curve: IMD: AUC = 0.58, p = 0.612; SPWMD: AUC 0.46, p = 0.71; TDId: AUC 0.63, p = 0.79; DLC AUC 0.60, p = 0.93; Ts-12 AUC = 0.88, p = 0.25; LVEMD AUC 0.56, p = 0.33, TS-12-SD AUC = 0.88 p = 0.01.Intra- and interobserver variability was calculated by the intra-class correlation coefficient (ICC). There were good correlations for Tissue Doppler measurements .The main result of this prospective pilot study is that prospective assessment of multiple echocardiographic parameters of asynchrony increases the success rate of CRT.In most large studies, patient selection was solely based on QRS width and NYHA class. Patient selection by echocardiographic parameters of asynchrony was only performed in a subset of studies for borderline cases ,8. The pHow can the improved responder rate in our study be explained? Firstly, as myocardial asynchrony is a complex phenomenon, every single parameter reflects one aspect of this pathology. Our parameters evaluate inter- and intraventricular asynchrony, 2D as well as TDI-echocardiography. Therefore, integrating different parameters in the selection process increases the chance to select patients with relevant asynchrony for CRT.Secondly, the improved response rate could be due to the single center design and the careful patient assessment and low inter- and intra-observer-variability. TDI measurements are susceptible to observer variability, subjective assessment of the curves and individual learning curves. This might limit the reliability of multi-center studies in CRT as in the PROSPECT study. Different echo machines and unclear definition of echo parameters might also have contributed to disappointing results.Thirdly, to our experience, it is difficult to rely on one parameter alone because, for example, the SPWD cannot be measured in patients with previous anterior and septal myocardial infarction. Furthermore, reduced acoustic windows limit certain measurements frequently.In our study, most parameters showed a non-significant trend of improvement. This could be due to the small patient number in our study. But this might also indicate that a single parameter does not have enough power to predict response to CRT.Two large studies have analyzed echocardiography in the prediction of CRT success: The PROSPECT and Re-THIN-Q study ,9. The pThe success rate of CRT is low (50.3–63.0%) when defined by LVESD reduction . The PROThe Re-THIN-Q study  evaluateWhich parameters contribute to patient selection for CRT? The optimal technology to measure myocardial asynchrony is still in debate. There is increasing concern about asynchrony measurement by TDI-velocity because of double-peaks and beat-to-beat variability of the curves which are subject to tethering and translational motion. Hence, some authors have suggested that strain and 2D strain derived measurements of asynchrony  might have a higher prognostic value -25. A reThe study by Bleeker  suggesteSuboptimal lead position can contribute to non-successful CRT. Studies have shown that optimal lead position in the site of the latest myocardial activation can improve the echocardiographic and clinical results ,28. In oIn summary, we conclude that the implementation of different markers of asynchrony seems to improve the hemodynamic response rate in this small single center study. To further support our findings, larger prospective, controlled and randomized multi-center studies will have to be performed in order to find an appropriate combination of parameters.This is a small pilot study performed in a single center. Due to the small number of patients, no multivariate analysis of the several parameters and no calculation of predictive values could be performed. We have not systematically examined myocardial scar burden by cardiac MRI prior to CRT implantation. The choice of echo parameters should include parameters of three-dimensional echo as well as parameters of radial and circumferential asynchrony. This was not done because the software and equipment was not available for all patients.CRT: cardiac resynchronization therapy; DLC: delayed longitudinal contraction; ICD: implantable cardioverter defibrillator ; IMD: interventricular electromechanical delay; LVEMD: left ventricular mechanical delay; ROC: Receiver Operator Characteristic; SPWMD: septal-to-posterior wall motion delay; TDI: tissue Doppler imaging; TDId: delay of the septal and basal time-to-peak velocity; Ts: time-to-peak systolic velocity; Ts-12: maximal difference in the time-to-peak velocities of 12 myocardial segments; Ts-12-SD: standard deviation of time-to-peak velocities of 12 myocardial segments; TSI: Tissue Synchronization Imaging;FK and SS equally contributed to the study. FK, SS, ACB, AG, CR, HJB, CM, HD, AP participated in contributions to conception, analysis and interpretation of data, the follow-up echocardiographic examinations and made comments to the manuscript. HB and CM implanted the CRT systems and analyzed data. BG has supervised and commented the study. ACB was the supervisor of echo examinations, is head of the echo lab, and contributed by revising the manuscript critically.The authors declare that they have no competing interests.Measurement of the IMD in the aortic and the pulmonary outflow tracts.Click here for fileM-mode in the paarasternal long axis to determine SPWMD.Click here for fileAssessment of Ts12 and Ts-12-SD by TSI.Click here for fileTSI: Patient with asynchrony in the lateral wall .Click here for fileTDId in a healthy control and the asynchrony of myocardial contraction in the septal and lateral basal segments.Click here for fileMeasurement of the LVEMD in the aortic outflow tract.Click here for fileApical four chamber view. Myocardial systolic displacement: Evidence for lateral apical wall delayed longitudinal contraction.Click here for file


In patients with myocardial infarction or heart failure, right ventricular (RV) dysfunction is associated with death, shock and arrhythmias. In patients with type 2 diabetes mellitus, structural and functional alterations of the left ventricle (LV) are highly prevalent, however, little is known about the impact of diabetes on RV characteristics. The purpose of the present study was to investigate whether LV changes are paralleled by RV alterations in a rat model of diabetes.18F]-2-fluoro-2-deoxy-D-glucose under hyperinsulinaemic euglycaemic clamp conditions. Glucose, insulin, triglycerides and fatty acids were assessed from trunk blood. Another group of rats received an insulin or saline injection to study RV insulin signaling.Zucker diabetic fatty (ZDF) and control (ZL) rats underwent echocardiography and positron emission tomography (PET) scanning using [M-value  and RV MRglu associated with M-value . Finally, reduced RV insulin-stimulated phosphorylation of Akt was found in ZDF vs. ZL (p < 0.05).ZDF rats developed hyperglycaemia, hyperinsulinaemia and dyslipidaemia . Echocardiography revealed depressed LV fractional shortening and tricuspid annular plane systolic excursion (TAPSE) in ZDF vs. ZL rats (both p < 0.05). A decrease in LV and RV insulin-mediated glucose utilisation was found in ZDF vs. ZL rats (both p < 0.05). LV associated with RV with respect to systolic function  and glucose utilisation . TAPSE associated with RV MRglu  and LV changes were paralleled by RV alterations in insulin-stimulated glucose utilisation and RV systolic function in a rat model of diabetes, which may be attributed to ventricular interdependence as well as to the uniform effect of diabetes. Since diabetic patients are prone to develop diabetic cardiomyopathy and myocardial ischaemia, it might be suggested that RV dysfunction plays a central role in cardiac abnormalities in this population. Although been underestimated in the past, the contribution of right ventricular (RV) function to overall myocardial contractility is considerable. RV dysfunction is relevant in a variety of disease states, like pulmonary hypertension, coronary heart disease and heart failure. RV dysfunction is an independent predictor of outcome in patients with myocardial infarction  and hearWhile left ventricular (LV) impairment is a common complication of type 2 diabetes mellitus (T2DM), the number of studies focusing on the impact of T2DM on RV function is limited and conflicting -8. We 99 and othAll experiments were approved by the Animal Care and Use Committee of the VU University, and were conducted following the European Convention for the Protection of Vertebrate Animals used for Experimental and Other Scientific Purposes, and the Dutch Animal Experimentation Act.Male Zucker diabetic fatty (ZDF) rats  and age-matched Zucker lean control rats  underwent echocardiography and positron emission tomography (PET) at 14 weeks of age. Trunk blood was collected for determinations of blood glucose, plasma insulin, fatty acid and triglyceride levels [(-11*[PAAT/cl]) -2-fluoro-2-deoxy-D-glucose (18FDG) PET under hyperinsulinaemic euglycaemic clamp conditions, a gold-standard estimate of whole-body insulin sensitivity [LV and RV glucose metabolism were measured using [sitivity . Quantifsitivity .Sections of LV and RV were stained with hematoxylin-eosin for determination of cardiomyocyte cross-sectional area . Picrosi-1 BW insulin) or saline as control  to study RV insulin signaling [A separate group of rats  received insulin stimulation , phospho-AMP activated protein kinase (AMPK)-Thr172, AMPK  and pyruvate dehydrogenase kinase-4  . All sigAll data are presented as mean ± SEM. Group comparisons were performed using student t-test or two-way ANOVA with Bonferroni post-hoc analysis. Correlations were calculated by the Pearson's test. p < 0.05 was considered as statistically significant.M-value was significantly lower in ZDF rats than in control rats  measured under hyperinsulinaemic euglycaemic conditions were decreased by 66% and 60%, respectively, in ZDF versus ZL rats Figure  and 1D. M-value  and RV MRglu associated significantly with M-value .TAPSE associated significantly with RV MRglu  and RV weight, RV/(LV + septum) ratio, LV weight and lung weight were similar in ZDF and ZL rats (data not shown). Cross-sectional areas of individual RV cardiomyocytes were similar between both groups, whereas cross sectionals areas of individual LV cardiomyocytes were significantly increased Figure  in ZDF rPhosphorylation of Akt and GSK3β were studied to determine RV insulin sensitivity. ZDF and ZL hearts showed similar basal Akt and GSKβ phosphorylation. RV insulin-dependent phosphorylation of Akt-Ser473 was decreased in ZDF rats  and AMP-activated kinase (AMPK) protein expression was decreased in ZDF rats compared to ZL rats, however, GLUT4 failed to reach significance  increased LV filling pressure is translated to the pulmonary circulation, 2) ventricular interdependence and 3) both ventricles are exposed to the metabolic abnormalities characterising T2DM. Measurements on afterload and RV remodeling remained unchanged; we can therefore conclude that there are no differences in pulmonary vascular resistance. Based on the geometry of the heart it is expected that there is ventricular interdependence. However, in a model of diet-induced obesity, impaired LV function in the absence of RV dysfunction was found (data not shown), which suggests that the effect of diabetes on RV function may be of greater importance than previously assumed. In combination with the Collectively, diabetes seems to affect RV glucose metabolism and RV systolic function in similar proportions as in the LV, which could be due to ventricular interdependence as well as the uniform effect of diabetes on the heart.Whereas consequences of diabetes on the heart were previously restricted to the LV, this study showed that LV insulin-stimulated glucose utilisation and LV systolic function are paralleled by significant alterations in RV insulin-stimulated glucose utilisation and RV function in an experimental rat model of diabetes. RV dysfunction is associated with worse outcome in a variety of cardiovascular diseases, including myocardial infarction and heart failure. The negative association of RV function with prognosis has only been scarcely investigated in the diabetic population. However, since diabetic patients are prone to develop diabetic cardiomyopathy and myocardial ischaemia , it mighThe authors declare that they have no competing interests.CEvdB participated in performing the study, data analysis, statistics and writing the manuscript. JWAM and RV in part performed the study. MLH contributed in interpretation of data. MCH and ML in part performed data analysis. CFMM in part performed the study and contributed to the design of the study. AAL in part participated in the design of the study and reviewed/edited the manuscript. DMO participated in the design of the study and reviewed/edited the manuscript. MD supervised the study, participated in the design of the study and reviewed/edited the manuscript. CB supervised the study and wrote/reviewed/edited the manuscript. All authors read and approved the final manuscript.