Postischemic Dilated Cardiomyopathy Research Articles

Efficacy and Safety of a Combined Aerobic, Strength and Flexibility Exercise Training Program in Patients with Implantable Cardiac Devices.

Purpose: The “FIDE Project” (Fitness Implantable DEvice) was organized by the Institute of Sports Medicine and Science and the World Society of Arrhythmias with the aim of demonstrating the usefulness of exercise training in improving functional capacity in patients with implantable cardiac devices. Materials and Methods: Thirty sedentary patients were selected for the project (25 males and 5 females), with a mean age of 73 ± 5 years (range 44–94 years). Twenty-five were implanted with a Pacemaker (PM) and five with an Implantable Cardioverter Defibrillator (ICD). Atrial fibrillation/atrial flutter was present in ten (34%) patients, post-ischemic dilated cardiomyopathy in five (17.2%), sick sinus syndrome in six (20,7%), complete atrium-ventricular block in six (20.7%), hypertrophic cardiomyopathy in one (3.4%) and recurrent syncope in one (3.4%). The baseline assessment comprised cardiovascular examination, resting and stress ECG, cardiopulmonary exercise testing (V ˙O2peak), strength assessment of different muscle groups, and a flexibility test. The same measurements were repeated after 15–20 consecutive training sessions, over a 2-month period. The exercise prescription was set to 70–80% of HRR (Heart rate reserve) and to 50–70% of 1RM (1-repetition maximum, muscular force). The training protocol consisted of two training sessions per week performed in our institute, 90 min for each (warm-up, aerobic phase, strength phase and stretching) and one or more at home autonomously. Results: The cardiopulmonary testing after the training period documents a significant improvement in V ˙O2peak (15 ± 4 mL/kg/min vs. 17 ± 4; p = 0.001) and in work load (87 ± 30 watts vs. 108 ± 37; p = 0.001). Additionally, strength capacity significantly increased after the cardiac rehabilitation program, (quadriceps: 21 ± 18 kg vs. 29 ± 16 kg, p = 0.00003). Flexibility tests show a positive trend, but without statistical significance (sit-and-reach test: −19 ± 11 cm vs. −15 ± 11.7 cm; back-scratch test: −19 ± 11.6 cm vs. −15 ± 10 cm; lateral flexibility right −44 ± 1.4 cm vs. −43 ± 9.5 cm; left −43 ± 5 vs. −45 ± 8.7 cm). Conclusion: A brief period of combined aerobic, strength and flexibility exercise training (FIDE project) proved to be effective and safe in improving functional capacity in patients with cardiac implantable devices.

P349 A REPRODUCIBLE SENSOR PATTERN TO SUSPECT COVID19 PULMONARY INFECTION WITH LATITUDETM. CASE REPORT AND LITERATURE REVIEW

A 78 year–old patient with post–ischaemic dilated cardiomyopathy and severely reduced ejection fraction was implanted with a Boston Scientific RESONATE X4 CRT–D and followed by LATITUDETM remote monitoring platform. From the end of January to the end of March 2021 he was hospitalized for COVID19 pneumonia followed by two episodes of acute heart decompensation. We remotely followed the patient and identified a specific Heart Logic sensor pattern linked to the COVID19 pneumonia: an increase of the thoracic impedance combined with an increase of the respiratory rate (RR), S1 heart sound and the nocturnal heart rate (nHR). This pattern differed from the one linked to the subsequent episodes of heart failure, characterized by a decrease of the thoracic impedance and of S1 heart sound combined with a high RR and nHR. We eventually made a literature review on the topic and found that our observations were in line with what was published: an increase in the thoracic impedance in association with an increase in the RR and a decrease in the activity level was present in the majority of published COVID19 patients followed by LATITUDETM remote monitoring platform. Furthermore a recent comparative study found that the thoracic impedance was significantly higher in COVID–19 patients as compared with acute HF patients, suggesting an underlying pathophysiological mechanism related to pulmonary infection.The present case and the literature review show that LATITUDETM remote monitoring algorithm may become a useful tool to remotely detect SARS–CoV–2 infection, distinguish it from HF and lead to an early hospitalisation for symptomatic patients or to a simple home monitoring.

P39 ATRIAL MASS IN HEART TRANSPLANTED PATIENT WITH CLINICAL HISTORY OF LYMPHOMA

Abstract Atrial thrombosis is an uncommon complication of cardiac transplant, especially when performed with standard technique. Pathogenetic mechanisms might involve atrial anatomy distortion and abnormalities in its contractile function, which induce flow stasis and thrombus formation, mostly on the surgical suture. A 77–year–old man underwent orthotopic heart transplantation in 2000 for post–ischemic dilated cardiomyopathy. In 2019 he was diagnosed with diffuse large B–cell lymphoma treated with chemotherapy. On March 2021, during follow up period, he had a total body CT scan which showed a submandibular space–occupying lesion, likely as a disease recurrence, and a large atrial mass (30x50 mm). For this reason, he was admitted to the emergency department. Echocardiography documented a massive hyperechogenic formation in an enlarged left atrium. In order to rule out a neoplastic nature, a cardiac CMR was performed, confirming the presence of an oval mass adhering to the posterior left atrial wall with partial involvement of pulmonary veins ostia, with inhomogeneous isointense signal on T1–weighted sequences and hyper–isointense signal on T2–weighted sequences, without significant contrast enhancement, likely representing an endoluminal thrombotic formation. Given the patient’s clinical status and his hemodynamic stability, a surgical excision was deferred. The patient was discharged on oral anticoagulant therapy with Warfarin (INR target 2–3). Three months later, a chest CT showed a meaningful mass reduction (11x18mm), which was no longer visible at echocardiography. About 9 months later, complete disappearance of the atrial mass was found at a CT scan. According to scientific literature, differential diagnosis of a newly discovered atrial mass in a transplanted heart includes thrombosis or neoplasia. Thrombosis occurs usually early after surgery, but due to promoting factors, it can arise after many years. The most likely triggering condition is an acquired prothrombotic status: in our case the likely lymphoma recurrence may have led to thrombogenesis. In order to exclude with confidence cardiac metastasis, histological examination would have been necessary. Nevertheless, the meaningful mass reduction, as early as three months after starting oral anticoagulation, and its disappearance nine months after, strongly suggests for atrial thrombosis.

778 Acute clinical valve thrombosis after transcatheter mitral valve-in-valve replacement

Abstract Aims Transcatheter heart valve (THV) thrombosis is a frequent and potentially life-threatening complication of transcatheter mitral valve replacement (TMVR), occurring in approximately 12% of patients (mainly within the first 3 months after the procedure). The majority of THV thromboses is non-obstructive and subclinical, and remains undetected until a routine echocardiogram is performed. Methods A 65 years old male was suffering from post-ischaemic dilated cardiomyopathy and severe left ventricle systolic dysfunction (LVEF 28%), secondary to a previous STEMI in 2010 treated with primary PCI on proximal LAD; after the STEMI he developed a left ventricle aneurysm and a subsequent severe secondary mitral regurgitation. In late 2020 he underwent a surgical valve replacement with a biologic valve (Perimount Magna Mitral Ease n. 27), alongside a left ventricle reshaping (Dor procedure). After a few months, the patient developed worsening dyspnoea and severe exercise intolerance; a transesophageal echocardiogram (TEE) showed an extensive valve degeneration with diffuse leaflet thickening determining severe valve stenosis and regurgitation. The patient was then admitted to the Cardiology department. A coronary angiography was performed, showing good result of previous PCI and excluding other critical stenoses. The patient then underwent a transcatheter valve-in-valve replacement with a Sapien S3 n. 29 in mitral position. The patient was already in chronic therapy with acetilsalicilic acid (ASA), and after the procedure anticoagulant therapy with Warfarin was started. In the post-procedural period the patient developed an acute worsening of the LVEF with severe hypotension, likely due to after-load mismatch; hence, supportive inotropic therapy with Adrenalin and Enoximone was required. A TEE performed 7 days after the procedure showed absence of diastolic excursion of posterior and lateral cusps and leaflet thickening with a 4 mm thrombotic apposition on the ventricular side, determining severe valve stenosis with markedly increased transvalvular gradients (peak gradient 20 mmHg, mean gradient 11 mmHg). A CT scan of the heart confirmed the valve thrombosis on the inferior and lateral leaflets. Results Unfractioned heparin (UFH) was then added to ASA and Warfarin (INR target of 3.0). After 11 days of aggressive antithrombotic therapy a new TEE was performed, showing marked reduction in transvalvular gradients (peak gradient 10 mmHg, mean gradient 5 mmHg) due to partial dissolution of the thrombotic formation. Warfarin was then stopped, and after switching from UFH to Enoxaparin the patient was discharged asymptomatic and in good general conditions, with indication of follow-up with TEE at 1 month. Conclusions Valve-in-valve TMVR is a relatively new and still infrequent procedure, therefore few evidences about its complications are currently available. Thrombosis on these valves is not rare (12%), but usually develops on the atrial side of the leaflets; interestingly, in this patient the thrombosis was on the ventricular side, likely due to an acute reduction in flow velocity caused by the after-load mismatch and the subsequent cardiogenic shock.

447 Left ventricular non-compaction with coronary artery anomaly: incidental diagnosis after ST-elevation myocardial infarction

Abstract Left ventricular noncompaction (LVNC) is a rare congenital cardiomyopathy thought to be caused by arrest of normal endomyocardial morphogenesis. A 33-year-old male, smoker, dyslipidemic not on medical therapy, with family history for sudden cardiac death (SCD) presented to the ER for chest pain radiated to the left arm, unrelated to exertion. The physical examination was within normal limits. Blood tests showed increased cardiac enzymes levels (Troponin I hs 49 308.7 ng/l). The EKG showed STE in the anterior leads and diffuse ventricular repolarization anomalies, suggestive of anterior STEMI. The patient underwent coronary catheterization, with evidence of anomalous origin of the Cx from the RCA and critical stenosis on the proximal LAD, treated with PPCI and implantation of a DES with good angiographic result. The patient was transferred to the Cardiac Intensive Care Unit. TTE showed moderate LV dilatation, severe LV dysfunction (EF 30%) with apical, septal and anterior wall akinesis, and lateral wall hypertrabecularization with multiple prominent trabeculations and deep intertrabecular recesses communicating with the cavity, suggestive for LVNC. Cardiac MRI documented dilated LV with EF 34%, anterior and antero-septal wall akinesis (associated with increased T1 mapping values and areas of LGE after contrast injection, compatible with ischaemic outcomes), infero-lateral wall hypokinesia and LV free wall marked hypertrabecularization with a ratio of not compacted(T)/compacted(M) myocardium of 5 (Petersen criteria for LVNC diagnosis: T/M > 2.3 in telediastolic long-axis view). The patient was discharged in stable clinical conditions in DAPT(Cardioaspirin and Ticagrelor). At two months cardiologic follow-up the patient was asymptomatic and TTE confirmed a dilated LV with severely depressed EF (30%). In consideration of the post-ischaemic dilated cardiomyopathy with severely depressed EF and of the family history of SCD (father deceased at 54-years-old), the patient was admitted in our Cardiology Unit and he underwent subcutaneous ICD (sICD) implantation. He was discharged in stable conditions with remote home monitoring transmitter. The association between LVNC and anomalous coronary artery origin is rare. LVNC is sometimes associated with coronary artery disease, but only rare cases of acute myocardial infarction have been described in literature, with exceptionally rare cases of LVNC incidental diagnosis after STEMI. To the best of our knowledge, this is the first case of LVNC associated with anomalous coronary artery origin and STEMI reported in literature. Some authors hypothesized that a single gene responsible for both myocardial development and coronary endothelium could be involved in the pathogenesis of LVNC and at the same time predispose to coronary atherosclerosis. Further studies are necessary in order to assess the possible pathophysiological mechanisms that correlate LVNC and coronary atherosclerosis. According to European guidelines, LVNC in the absence of additional risk factors is not an indication for primary ICD implantation, and for arrhythmic risk stratification it’s recommended to follow the criteria used for non-ischaemic dilated cardiomyopathy. The anomalous origin of the Cx from the RCA has an incidence of 0.37%, and it is generally not linked to an increased risk of SCD. Involvement of RV in LVNC cannot be excluded even when RV appears normal on CMR, and if involved there is higher risk of perforation by the lead. sICD overcomes disadvantages of transvenous ICD in patients without a need for pacing therapy. In literature use of sICD is reported only in 14 patients with LVNC, mainly children and young adults.

Challenging Transcatheter Treatment of a “Complex” Refractory Congestive Heart Failure

A 61-year-old man with a history of postischemic dilated cardiomyopathy was referred in advanced congestive heart failure to our department (Department of Cardiology). He had a history of acute inferolateral myocardial infarction complicated by left ventricular (LV) aneurysm treated elsewhere by coronary artery bypass grafts, aneurysm resection, and automatic implantable cardioverter defibrillator implantation a few years before. At the time of admission, he was in functional New York Heart Association class III-IV with signs and symptoms of congestive heart failure and low cardiac output.

A common polymorphism in the SCN5A gene is associated with dilated cardiomyopathy.

AimsSCN5A is a disease-causing gene associated with familial dilated cardiomyopathy (FDC). We examined the possible association between a common polymorphism in the SCN5A gene (c.1673A>G-p.H558R; rs1805124) and the risk of dilated cardiomyopathy (DCM) occurrence.MethodsWe genotyped 185 DCM cases (familial DCM, idiopathic DCM and postischemic DCM) and 251 controls for the p.H558R polymorphism in the SCN5A gene, to test the association of the molecular epidemiology of the individuals with the presence/absence of various types of DCM.ResultsOur results showed that the rs1805124 polymorphism was significantly associated with DCM, and the association was more significant in patients with FDC; furthermore, in these individuals, the less frequent GG genotype was associated with a 7.39-fold increased risk of disease [95% confidence interval (95% CI) = 2.88–18.96; P < 0.0001] compared with the AA genotype. Moreover, logistic regression analysis showed that GG carriers had a higher risk of DCM than AA + AG carriers (odds ratio = 5.45, 95% CI = 2.23–13.35; P < 0.001). No association was observed between the rs1805124 and DCM risk in postischemic DCM patients.ConclusionOur study demonstrates an association between familial DCM and the rs1805124 polymorphism in the SCN5A gene, which may unravel additional genetic predisposition to the development of a multifactorial disease as DCM.

Assessment of Remote Myocardium Heterogeneity in Patients with Ventricular Tachycardia Using Texture Analysis of Late Iodine Enhancement (LIE) Cardiac Computed Tomography (cCT) Images

PurposeDiffuse remodeling of myocardial extra-cellular matrix is largely responsible for left ventricle (LV) dysfunction and arrhythmias. Our hypothesis is that the texture analysis of late iodine enhancement (LIE) cardiac computed tomography (cCT) images may improve characterization of the diffuse extra-cellular matrix changes. Our aim was to extract volumetric extracellular volume (ECV) and LIE texture features of non-scarred (remote) myocardium from cCT of patients with recurrent ventricular tachycardia (rVT), and to compare these radiomic features with LV-function, LV-remodeling, and underlying cardiac disease.ProceduresForty-eight patients suffering from rVT were prospectively enrolled: 5/48 with idiopathic VT (IVT), 23/48 with post-ischemic dilated cardiomyopathy (ICM), 9/48 with idiopathic dilated cardiomyopathy (IDCM), and 11/48 with scars from a previous healed myocarditis (MYO). All patients underwent echocardiography to assess LV systolic and diastolic function and cCT with pre-contrast, angiographic, and LIE scan to obtain end-diastolic volume (EDV), ECV, and first-order texture parameters of Hounsfield Unit (HU) of remote myocardium in LIE [energy, entropy, HU-mean, HU-median, standard deviation (SD), and mean absolute deviation (MAD)].ResultsEnergy, HU mean, and HU median by cCT texture analysis correlated with ECV (rho = 0.5650, rho = 0.5741, rho = 0.5068; p < 0.0005). cCT-derived ECV, HU-mean, HU-median, SD, and MAD correlated directly to EDV by cCT and inversely to ejection fraction by echocardiography (p < 0.05). SD and MAD correlated with diastolic function by echocardiography (rho = 0.3837, p = 0.0071; rho = 0.3330, p = 0.0208). MYO and IVT patients were characterized by significantly lower values of SD and MAD when compared with ICM and IDCM patients, independently of LV-volume systolic and diastolic function.ConclusionsTexture analysis of LIE may expand cCT capability of myocardial characterization. Myocardial heterogeneity (SD and MAD) was associated with LV dilatation, systolic and diastolic function, and is able to potentially identify the different patterns of structural remodeling characterizing patients with rVT of different etiology.

Case Report: Aortic Valve Replacement After JARVIK 2000 Left Ventricular Assist Device Implantation in Long-Time Survivor With Severe Aortic Valve Regurgitation

BackgroundThere are limited clinical records in the literature regarding aortic valve replacement in left ventricular assist device (L-VAD) patients. Previously we had two cases of severe aortic valve regurgitation in patients with L-VAD support treated with Corvalve prosthesis insertion and Amplatzer closure procedure. Both patients died a few days after the procedure from complications not related to the procedure itself. Patient HistoryThe patient was a male with previous coronary artery bypass graft surgery in 2001 that was complicated with postischemic dilated cardiomyopathy with severe heart failure (ejection fraction [EF], 20%). Cardiac resynchronization therapy was biventricular-pacemaker and cardiac defibrillator implantation in 2009 for recurrent ventricular arrhythmia. L-VAD implantation (Jarvik 2000) with graft apposition in descending thoracic aorta through left thoracotomy access and retro-auricolar cable was performed in October 2013. In 2015 the patient underwent surgical aortic valve replacement with bioprothesis due to progressive worsening of the aortic valve regurgitation. The Jarvik 2000 outflow was occluded with vascular ball occluder inserted via right axillary artery under fluoroscopy before CEC installation. The recovery was without major complications. DiscussionLong-time survivors with Jarvik 2000 are increasing in number and such late complication is expected to become a main future issue. Our previous experience with the interventional approach was delusive. Due to the fatal consequences in similar patients with nonsurgical approaches, we opted for surgical aortic valve replacement. At the moment, the international literature does not describe safe approaches regarding aortic valve replacement in patients with Jarvik 2000 L-VAD. This case shows that surgical valve replacement could be managed with success according to the described specific technique.

Endoscopic guide wire gallbladder decompression in a critically ill, septic patient

A 57-year-old man with postischemic dilated cardiomyopathy underwent a heart transplant at our center in February 2013. His early postoperative course was complicated by primary graft non-function requiring intensive care treatment. Six days after transplantation, he developed severe hypoperfusion that required maximal extracorporeal membrane oxygenation (ECMO), placement of an intra-aortic balloon pump, and vasoactive drug support.

Influence of myocardial viability on responsiveness to cardiac resynchronization in ischemic dilated cardiomyopathy: a prospective observational cohort study

To understand whether patients with post-ischemic dilated cardiomyopathy and myocardial viability (MV) could benefit from cardiac resynchronization therapy (CRT) in terms of clinical, echocardiographic and neuro- hormonal parameters compared to patients without MV. One hundred and four consecutive patients were enrolled in a prospective observational cohort study. Using dobutamine stress echocardiography, 2 groups were identified: group A of 51 patients with MV and group B of 53 patients without MV. All patients were implanted with biventricular pacing devices combined with an internal cardioverter-defibrillator. Clinical, echocardiographic and neuro-hormonal parameters were evaluated at baseline and at six month follow-up. Analysis of variance for repeated measures on each variable suggestive of remodeling was performed. We considered responder every patient with: decrease of > 15% in left ventricular volumes and/or improvement in left ventricular ejection fraction of > 5% in addition to NYHA class improvement. All the variables improved in both groups (time effect). Comparing the two groups (group effect), the following variables were significantly better in group A: N-terminal pro-B-type natriuretic peptide (p=0.02), NYHA class (p=0.003), reverse remodeling (RR) (p=0.007), dP/dt (p=0.005), left ventricular ejection fraction (p=0.009), 3rd sound (p=0.01), and left ventricular end-systolic volume after the first week (p=0.035). RR occurred at the first week after CRT only in Group A and was maintained for all the time of this study. The maximum difference of the decrease of left ventricular volumes between the two groups occurred after the first week (p<0.001). Patients with MV responded better than patients without MV with a significant improvement after the first week from CRT.

Effects of pink grapefruit juice on QT variability in patients with dilated or hypertensive cardiomyopathy and in healthy subjects

Recent evidence shows that pink grapefruit juice, which is a recommended dietary addition that contains high amounts of the antioxidant flavonoid naringenin, prolongs the corrected QT (QT(c)), a noninvasive electrophysiological marker of spatial myocardial repolarization, and does so by inhibiting the rapid component of the delayed rectifier K+ current (I(Kr)). Prompted by the observation that all class III antiarrhythmic drugs inhibit this current, thereby sometimes provoking torsades de pointes, we compared the effects of a liter of freshly squeezed pink grapefruit juice with those of 2 commonly used class III antiarrhythmics amiodarone and sotalol on the major noninvasive markers of temporal variability in myocardial repolarization used to stratify the risk of sudden death from malignant ventricular arrhythmias. In 32 subjects, 10 with postischemic dilated cardiomyopathy, 12 with hypertensive cardiomyopathy, and 10 healthy, we assessed QT(c) and QT variability index (QTVI) after administration of fresh pink grapefruit juice, placebo, amiodarone, or sotalol. After pink grapefruit juice and sotalol, all these indexes increased significantly from values observed after placebo (P<0.05) and from values after amiodarone (P<0.05). Conversely, after amiodarone, QT(c), but not QTVI, increased significantly from values after placebo (P<0.05). Presumably because of its high naringenin glycoside content, pink grapefruit juice prolongs cardiac repolarization and concurrently increases temporal cardiac repolarization dispersion. The potential proarrhythmic actions of pink grapefruit juice might be of concern in patients with major myocardial structural disorders.

Influence of vitamin C on baroreflex sensitivity in chronic heart failure.

Chronic heart failure (CHF) reduces baroreflex sensitivity. Low baroreflex sensitivity, a risk factor for sudden death, could arise partly from CHF-dependent endothelial dysfunction. Vitamin C at high doses has a protective role against CHF-related endothelial damage. This study was conducted to investigate the effect of vitamin C on baroreflex sensitivity in CHF. A study group of 33 subjects with CHF secondary to postischemic dilated cardiomyopathy with an ejection fraction </=35% and a control group (11 subjects) underwent assessment of baroreflex sensitivity by the phenylephrine method and an autonomic nervous system study by power spectral analysis. Variables were assessed after infusion of placebo and high doses of vitamin C (2.5 mg). In subjects with CHF, baroreflex sensitivity was significantly higher after vitamin C than after placebo infusion (placebo: 4.1+/-0.4 versus vitamin C: 5.3+/-0.5 ms/mm Hg, P<0.001). Low-frequency of R-R (LFRR), expressed in normalized units (NU) (P<0.05); LF/high-frequency (HF) ratio (P<0.05), and LF of SBP (LFSBP) decreased significantly; HF power (P<0.05), and alpha-HF (P<0.001) increased. Conversely, in the control group, baroreflex sensitivity and other spectral variables measured at baseline, after placebo, and after vitamin C infusion remained statistically unchanged (placebo: 10.2+/-0.1 versus vitamin C: 10.0+/-0.2 ms/mm Hg, NS). Acute administration of vitamin C at high doses improves baroreflex sensitivity and vagal sinus modulation in patients with CHF. This finding could have notable clinical and therapeutic implications. Key issues to understand are whether the beneficial effect persists during chronic administration and whether it helps to improve survival.

Survival, haemodynamics and cardiac remodelling follow up in mice after myocardial infarction.

1. In the present study, the time-course, over a 1 year period, of postischaemic dilated cardiomyopathy and/or development of congestive heart failure was investigated in mice in terms of survival and cardiac functional and structural characteristics. 2. C57BL/6 mice with myocardial infarction (MI mice; coronary ligation n = 78) or sham-operated animals (n = 45) were used and echocardiographic, haemodynamic and histomorphometric parameters were assessed at 3, 6 and 12 months post-MI. 3. At 12 months, the survival rate was 70% in MI mice. Left ventricular dysfunction was evidenced by a strong decrease in ejection fraction (EF; -48 and -53% at 6 and 12 months, respectively; both P < 0.05) and an increase in left ventricular end-diastolic pressure (+100% at both 6 and 12 months; both P < 0.05). There was no major worsening in cardiac function between 6 and 12 months, suggesting strong compensatory mechanisms. Cardiac remodelling was observed, characterized by strong left ventricular hypertrophy (+38 and +62% at 6 and 12 months, respectively; both P < 0.05) and dilatation (+53% at 6 months; P < 0.05), but collagen was not significantly increased. Significant correlations were found between EF (echocardiography) and dP/dtmax, between end-diastolic volume (echocardiography) and left ventricular internal perimeter (histomorphometry) and between left ventricular mass (echocardiography) and weight. 4. In conclusion, despite a high survival rate, the MI mouse model displays most of the hallmarks of postischaemic dilated cardiomyopathy and/or congestive heart failure, thus affording the necessary background for the subsequent evaluation of gene manipulation and/or drug effects. In addition, two-dimensional echocardiography appears to be a suitable tool for the long-term follow up of cardiac function and remodelling in this model.