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A patient with severe heart failure secondary to coronary heart disease is presented. Following investigation he was thought to have significant areas of myocardial hibernation and was therefore treated with coronary revascularisation, with major clinical benefit.
In this study, 9 cases of tachycardia-induced cardiomyopathy have been reported, with a 7-year follow-up period. The patient population consisted of 5 males and 4 females with a mean age of 41 +/- 18 years (range: 10-70 years). It was difficult to determine the onset of the arrhythmia, due to its frequently asymptomatic course until such time as cardiac insufficiency became apparent (this was the case in 7 patients, while 2 subjects had palpitations). Four cases of AV intranodal reentry tachycardia (3 with an accessory pathway), 2 cases of atrial fibrillation, 1 case of auricular flutter, 1 case of atrial tachycardia and 1 case of ventricular tachycardia were observed. Disappearance of the symptomatology following restoration of sinus rhythm was accompanied by echocardiographically-determined normalization of systolic function on average 5 +/- 4 months post-arrhythmia (range: 1-12 months). Left-ventricular end-diastolic volumes decreased from 60 +/- 5 mm to 51 +/- 4 mm (P < 0.01), and end-systolic volumes from 50 +/- 7 mm to 35 +/- 4 mm (P < 0.001), while the left ventricular shortening fraction increased from 17 +/- 5% to 33 +/- 4% (P < 0.0001). In the differential diagnosis for primary dilated cardiomyopathy, tachycardia-induced cardiomyopathy appears very similar to the former, and only an adequate period of follow-up after the restoration of sinus rhythm can confirm the diagnosis.
Ischemic heart disease, once limited to a number of well defined entities such as angina of effort, unstable angina, and myocardial infarction, must now be regarded as a much more complex and elusive entity. Silent ischemia was the first of the new ischemic syndromes to be described. Recently, three further new syndromes have been added, namely stunning, hibernation and preconditioning. All three have one common theme--they can be related to ischemia and reperfusion. In stunning, there is post-reperfusion mechanical dysfunction that recovers. In hibernation, there is prominent contractile dysfunction, apparently out of proportion to the reduction in coronary flow, and the recovery upon reperfusion is good. In preconditioning, severe ischemia followed by reperfusion protects against subsequent ischemia which may modify the severity of ischemic damage in the other ischemic syndromes. Ischemic LV dysfunction as found in post-infarct patients and in the absence of any simple relation to reperfusion, can be either diastolic or systolic or both in nature. In ischemic LV diastolic dysfunction without major systolic dysfunction, calcium antagonists may be appropriate therapy which could point to a role for abnormalities in the regulation of cytosolic calcium. It is proposed that there is potentially a mixed post-infarct syndrome, which may comprise one or more of the new ischemic syndromes (silent ischemia, stunning, hibernation, and preconditioning), as well as a varying degree of systolic and/or diastolic dysfunction. The basis of the systolic dysfunction is, at least in part, post-infarct LV remodeling. Several of these entities could overlap in the same patient. The term "mixed post-infarct ischemic syndrome" is suggested to describe this condition.
Angiotensin-converting enzyme (ACE) inhibitors have been used for more than a decade in the treatment of chronic congestive heart failure. In recent years these agents have been used in patients who survived a myocardial infarction. However, primary care providers are often confused as to which patients would benefit the most, and as a result, these life-prolonging drugs are underutilized. The results of randomized controlled trials evaluating ACE inhibitors' effect on morbidity and mortality in patients with chronic congestive heart failure or acute myocardial infarction were evaluated. Angiotensin-converting enzyme inhibitors clearly improve survival in patients with symptomatic congestive heart failure. This survival benefit is approximately 6 months. In patients with asymptomatic systolic dysfunction, these agents also decrease the number of hospital admissions due to heart failure. Angiotensin-converting enzyme inhibitors also improve survival in all patients who experienced an acute myocardial infarction. With the plethora of evidence regarding the positive effects that this class of drugs has on the quality of life and survival of patients with systolic dysfunction, it is still unclear why clinicians are reluctant to use them more often. Primary care providers need to be educated on how to risk stratify patients to make this therapy more cost effective, and when these agents should be started.
The criteria required for the diagnosis of the four clinical aspects of the congestive heart failure, that are needed for the correct management of patients are discussed: the diagnosis of the syndrome, mechanism (systolic or diastolic dysfunction), ethology and functional capacity. The "initial evaluation" of patients presenting with symptoms of heart failure is described to encourage an structured diagnostic approach and the cost/effective use of diagnostic methods.
OBJECTIVE: Trimetazidine has been shown to have anti-ischemic properties by improving exercise tolerance without haemodynamic effects and direct cyto-protective effects on the myocardium. The aim of this study was to assess the effect of trimetazidine on the treatment of patients with ischemic cardiomyopathy, and to assess the anti-angina efficacy and the clinical tolerance of TMZ. METHODS: 60 ischemic cardiomyopathy patients on conventional therapy were enrolled in this open multiple center clinical trial and received TMZ (20 mg 3 times per day) for six months. Patients were followed up for six months and assessments included clinical evaluation, electrocardiography and echocardiography. RESULTS: All patients tolerated 60 mg of trimetazidine for six months, left ventricular ejection fraction (LVEF) was increased from 32.4 +/- 6.3% to 41.8 +/- 10.8% (P < 0.0001). Stage of NYHA classification was improved in most patients (P < 0.0001). Attack of angina was relieved and consumption of nitroglycerin reduced (both P < 0.001). CONCLUSION: Trimetazidine seems to improve clinical status and ejection fraction, and reduce angina onsets without adverse effects in patients with ischemic cardiomyopathy.
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BACKGROUND: Although patients with heart failure express elevated circulating levels of tumor necrosis factor-alpha (TNF-alpha) in their peripheral circulation, the structural and functional effects of circulating levels of pathophysiologically relevant concentrations of TNF-alpha on the heart are not known. METHODS AND RESULTS: Osmotic infusion pumps containing either diluent or TNF-alpha were implanted into the peritoneal cavity of rats. The rate of TNF-alpha infusion was titrated to obtain systemic levels of biologically active TNF-alpha comparable to those reported in patients with heart failure (approximately 80 to 100 U/mL), and the animals were examined serially for 15 days. Two-dimensional echocardiography was used to assess changes in left ventricular (LV) structure (remodeling) and LV function. Video edge detection was used to assess isolated cell mechanics, and standard histological techniques were used to assess changes in the volume composition of LV cardiac myocytes and the extracellular matrix. The reversibility of cytokine-induced effects was determined either by removal of the osmotic infusion pumps on day 15 or by treatment of the animals with a soluble TNF-alpha antagonist (TNFR:Fc). The results of this study show that a continuous infusion of TNF-alpha led to a time-dependent depression in LV function, cardiac myocyte shortening, and LV dilation that were at least partially reversible by removal of the osmotic infusion pumps or treatment of the animals with TNFR:Fc. CONCLUSIONS: These studies suggest that pathophysiologically relevant concentrations of TNF-alpha are sufficient to mimic certain aspects of the phenotype observed in experimental and clinical models of heart failure.
OBJECTIVE: The purpose of this study was to identify echocardiographic parameters that allow distinguishing different levels of cardiac dysfunction in aortic banded rats. METHODS: Wistar male rats (90-100 g) were subjected to aortic banding (n=23) or a sham operation (n=12). The following echocardiographic parameters were evaluated and used to group rats into groups with similar characteristics using cluster analysis: absolute values and after normalization to body weight of left ventricular end-diastolic diameter (LVDD) and left atrial systolic diameter; left ventricular end-systolic diameter (LVSD); LV weight to body weight ratio (LVW/BW); three indexes of left ventricular shortening (endocardial fractional shortening, EFS; midwall FS, MFS; and posterior wall shortening velocity, (PWSV). RESULTS: The cluster analysis could group aortic banded rats into two groups: mild (n=13) and severe (n=9) stage of heart failure. There was no overlapping among the values of the 95% confidence interval of the following parameters between the two groups: LVDD, LVSD, EFS, MFS, LVW/BW, and PWSV. CONCLUSION: It is feasible to distinguish two groups of aortic banded rats according to the level of cardiac dysfunction using those echocardiographic parameters. This allows to perform longitudinal studies in homogeneous groups of rats with aortic banding and cardiac dysfunction.
A series of elegant experimental studies and careful clinical observation over a decade or more have led to the concept of 'infarct expansion' and 'remodelling' of the heart, culminating in a number of major mortality studies indicating the effectiveness of angiotensin-converting enzyme (ACE) inhibitors in patients after myocardial infarction (MI). But has this concept been too narrow in predicting which patients might benefit from treatment with ACE inhibitors? Measurable infarct-expansion with progressive dilatation probably occurs in less than 20% of patients, whereas increase in volume and hypertrophy of the heart as responses to compromised function are likely wherever significant myocardial damage has occurred. Irrespective of infarct expansion, cumulative extensive damage can lead to an inevitable downward spiral with gross ventricular dilatation and death in heart failure. But in the majority of patients after MI a 'new equilibrium' is established in which initial dilatation and subsequently hypertrophy restore adequate function. Is it possible to distinguish patients in whom the cost and inconvenience of long-term therapy with an ACE inhibitor justify the likely benefit from treatment after an MI? The SAVE, AIRE and recent TRACE studies allow a rational approach for the clinician, indicating the effectiveness of these drugs in patients with evidence of impaired ventricular function. However, the prospect that ACE inhibitors prescribed long term might also prevent myocardial reinfarction could justify wider use. Post-MI patients are an easily identifiable high-risk group for a cost-effective programme of secondary prevention. Reinfarction in an already damaged ventricle carries a particularly poor prognosis and its prevention by ACE inhibitors could make a major contribution to the undoubted benefit from these agents. The recently completed TRACE study with its long-term follow-up may help resolve this issue, which is also being investigated in a number of long-term prospective studies in populations at high risk of cardiovascular disease.
UNLABELLED: The aim of this study was to evaluate LV function, by means of echocardiography, after mitral valve repair (MVr) or mitral valve replacement (MVR) in patients (pts) with chronic degenerative mitral regurgitation (MR) and depressed LV systolic function during a 6-years follow-up (FU) period. PATIENTS AND METHODS: Forty-five pts with moderately severe or severe MR and preoperative EF<or=50% were divided into 2 groups: MVr group (27 pts, 19 men-8 women, aged 62+/-10 years) and MVR group (18 pts, 8 men-10 women, aged 60+/-12 years). The cause of MR was myxomatous mitral valve disease (MVr/MVR: 16/8), endocarditis (0/4) and degenerative mitral valves with ruptured chordae tendineae (11/6). All pts underwent transthoracic echocardiography preoperatively, postoperatively and annually during the FU period (6+/-3 years). RESULTS: In MVr group, 5 pts died, 5 were lost to FU and 2 pts underwent MVR due to MVr failure. In MVR group, 6 pts died, 3 were lost to FU and 1 was re-operated due to prosthetic valve endocarditis. Atrial fibrillation was similar between the 2 groups. MVr pts demonstrated significant LVEDD decrease postoperatively which was persistent during FU (p<0.05). LVESD also decreased (p<0.05), VTI improved (p<0.05), while FS and EF showed a trend to improve. In MVR pts, LVEDD was decreased (p<0.05) but increased during FU (p<0.05) and LVESD remained high, resulting in a decrease of FS and EF (p<0.05). VTI remained unchanged (p=NS). CONCLUSION: MVr in pts with non-ischemic MR and preoperative LV dysfunction achieves better preservation of LV systolic indices than MVR, probably due to preservation of the subvalvular apparatus and LV geometry.
In patients with heart failure, carvedilol ameliorated cardiac function, but it did not affect oxygen uptake, kinetics, and ventilatory efficiency during 6-minute exercise at a constant 50-W workload. Persistence of respiratory incompetence may prevent improvement in submaximal oxygen uptake kinetics.
BACKGROUND: The extent of myocardial scarring of the left ventricle (LV) is important in patients with chronic ischemic heart disease (CIHD). With delayed-enhancement magnetic resonance imaging (DE-MRI), scarred myocardium (hyper-enhanced) is easily distinguishable from viable (dark) myocardium. This investigation assessed the use of DE-MRI for predicting functional improvement after coronary artery bypass grafting (CABG) in patients with CIHD and significant LV dysfunction. METHODS: The patient population (n = 29) with CIHD and LV dysfunction (ejection fraction 28% +/- 10%) underwent both DE-MRI, to delineate scarred regions before revascularization, and echocardiography (Echo), to assess segmental function before and after CABG (interval 188 +/- 57 days). Using a 16-segment model, LV myocardium was semiquantitatively analyzed for scarring based on DE-MRI and for improvements in resting function by pre- and post-CABG Echo. RESULTS: Before CABG, 82% of targeted myocardial segments had abnormal contraction; 78% showed scarring, including 38% with greater than mild amounts (25%-100%). Normal contraction was found in 18% of segments before revascularization; scarred areas were identified in 42%, 84% of which had, at most, minimal amounts (0%-24%). Of segments with pre-CABG dysfunction, 82% with no evidence of scar recovered, compared to only 18% with > or =50% scarring. Amount of hyper-enhancement was a very good indicator of improvement of function, especially at the > or =50%/segment threshold; overall accuracy was 0.74 (95% CI 0.66-0.82, P <.001). CONCLUSIONS: In patients with CIHD and significant LV dysfunction, DE-MRI can predict likelihood of functional improvement after revascularization.
Patients with severe cystic fibrosis can develop cor pulmonale, but little is known about the function of the right ventricle (RV) early in the disease. We hypothesized that such patients might have subclinical RV dysfunction, detectable by tissue Doppler echocardiography, and related to the severity of lung disease. We studied 21 clinically stable patients (Group 1), five patients with severe lung disease (Group 2), and 23 age-matched healthy subjects. Patients had impaired RV systolic function. The mean (SD) systolic velocities of the RV free wall were 8.9 (1.7) cm/s in Group 1, 7.7 (1.0) in Group 2, and 10.8 (1.9) in healthy subjects (p < 0.001). The velocities of the tricuspid annulus were less in patients (p < 0.0001). Patients had a greater isovolumic relaxation time (p < 0.001), indicating RV diastolic dysfunction. RV wall thickness was greater in patients (0.4 [0.1] versus 0.3 [0.1] cm/m(2), p < 0.01). RV systolic function was related to C-reactive protein (r = - 0.66, p < 0.001) and FEV(1) (r = 0.62, p = 0.003) and diastolic function to interleukin-6 (r = 0.64, p < 0.005). Patients with cystic fibrosis have subclinical RV dysfunction, which correlates with the severity of lung disease. Tissue Doppler echocardiography provides a quantifiable indicator useful for detection and monitoring of disease progression.
We report the case of a 21 year-old patient with arrhythmogenic right ventricular dysplasia manifested by episodes of QRS tachycardia greater than 0.12 sec and isolated dysfunction of the right ventricle. The patient treated with amiodarone however, the tachycardia episodes persisted. The surface electrocardiogram showed left branch block with the axis down, which suggested a right ventricle origin, and was therefore considered an arrhythmogenic dysplasia. Echocardiography and cardioangiography showed alterations in the anatomy of the outflow tract of the right ventricle. A myocardial gammagraphy revealed no perfusion alterations. The endomyocardial biopsy showed perivascular fibrosis. An electrophysiology study was performed, stimulating the outflow tract of the right ventricle, which induced two types of ventricular tachycardias, one of them identical to that recorded clinical. The patient was treated with sotalol, and has been being free of ventricular tachycardia episodes for 18 months of follow-up. We consider that this entity should be studied in a systematic way in those patients with ventricular tachycardia originated in the outflow of the right ventricle and with primary cardiac illness.
In this paper, some controversial points regarding myocardial its definition hibernation are discussed, including its definition (improvement in contractility versus improvement in clinical or functional status or in prognosis), the histology and pathophysiology (dedifferentiation versus cellular degeneration) and the responses to the diagnostic methods more currently utilised, stress echocardiography and myocardial perfusion scintigraphy. The predictor factors for recovering after revascularization are also discussed.
Thirty patients with stable angina pectoris and ischemia on stress perfusion imaging underwent continuous ambulatory left ventricular (LV) function monitoring. Mental stress was induced by mental arithmetic. Fifteen patients developed transient LV dysfunction during mental arithmetic. Patients were followed for 2 years for adverse cardiac events. Twelve patients had cardiac events over 1 year (myocardial infarction in 4, and unstable angina in 8). Nine of 15 patients (60%) with and only 3 of 15 (20%) without mental stress-induced LV dysfunction developed cardiac events (p = 0.025). A higher proportion of patients with cardiac events were taking beta blockers (p = 0.01) and had lower resting heart rates (p = 0.002) than those without cardiac events. There was no difference in the baseline characteristics between the groups of patients with and without cardiac events. At 2-year follow-up, 10 of 15 patients (67%) with mental stress-induced LV dysfunction had adverse events compared with only 4 of 15 (27%) with no mental stress-induced LV dysfunction (p = 0.025). Thus, in this cohort of patients with stable angina pectoris, mental stress-induced LV dysfunction was associated with higher cardiac events on follow-up. The exact mechanism of this association is not clear. Mental stress may be a trigger for adverse cardiac events in these patients. Transient LV dysfunction in response to mental stress may be a marker of abnormal cardiovascular reactivity to emotional and psychological stimuli in patients with coronary artery disease and may be useful for risk stratification.
Churg-Strauss syndrome is a rare disorder characterized by hypereosinophilia and a systemic vasculitis occurring inpatients with asthma and allergic rhinitis. Vasculitis commonly affects the lungs, the heart, the skin, and the peripheral nervous system. Cardiac involvement is characterized by acute and constrictive pericarditis, myocarditis and endocarditis, as well as ischemic cardiomyopathy. Endomyocardial fibrosis similar to Loeffler's syndrome has been rarely described. In the presented case, a 43 year old man with a history of allergy and asthma suffered from increasing dyspnea, fever, pulmonary infiltates and cardiomyopathy. Laboratory studies were notable for marked hypereosinophilia. In a bronchoscopic lavage and transbronchial biopsy eosinophilic infiltrates accompanied by vasculitis were found, Churg-Strauss syndrome was diagnosed. Echocardiogram showed endomyocardial deposits in the apex of the right ventricle, right ventricular function was normal particular in the basal segments. The left ventricle was slightly enlarged and left ventricular function was impaired. The diastolic mitral in-flow showed a restrictive pattern. Additionally, a pericardial effusion was observed without signs of tamponade. The patient received corticosteroids, cyclophosphamide and cardiomyopathy-specific therapy and showed a marked improvement after 4 months.