ramipril and Cardiomyopathy--Dilated

Several cardiac biomarkers, especially brain natriuretic peptide (BNP) and N-terminal (NT)-proBNP, have been used as predictors of prognosis and negative remodeling in DCM. In the present study, we aimed to evaluate the prognostic value of tenascin-C in dilated cardiomyopathy (DCM) and whether it can be used to determine reverse remodeling in patients with DCM.. Sixty-six patients with DCM were followed up for 12 months after initiation of medical treatment including carvedilol, ramipril (candesartan if ramipril was not tolerated), spironolactone, and furosemide. Tenascin-C and NT-proBNP measurements and transthoracic echocardiography were performed at baseline and at 12 months.. At 12 months, a significant improvement in New York Heart Association class (2.57 ± 0.6 vs. 1.87 ± 0.5; P < 0.0001), left ventricular end-diastolic volume (217 ± 47 vs 203 ± 48; P < 0.0001), left ventricular ejection fraction (29.1 ± 5.5 vs 30.9 ± 3.8; P < 0.0001), NT-proBNP (2019 ± 558 vs 1462 ± 805; P < 0.0001), and tenascin-C (76 ± 19 vs 48 ± 28; P < 0.0001) values were observed, compared with baseline. Importantly, decrease in tenascin-C values were correlated with increase in left ventricular ejection fraction. Tenascin-C (odds ratio [OR], 1.896; <95% confidence interval [CI], 1.543-2.670; P = 0.02), diabetes mellitus (OR, 2.456; G95% CI, 1.987-3.234; P = 0.01) and hypertension (OR: 2.106, <95% CI, 1.876-2.897; P = 0.03) were independent predictors of mortality in patients with DCM.. Reverse ventricular remodeling obtained with carvedilol, ramipril/candesartan, and spironolacton is associated with decreases in left ventricular end-diastolic volume, left ventricular end-systolic volume, tenascin-C levels, and NT-proBNP levels. Consequently, tenascin-C may be used to evaluate reverse remodeling in patients with DCM.

Topics: Aged; Antihypertensive Agents; Benzimidazoles; Biphenyl Compounds; Carbazoles; Cardiomyopathy, Dilated; Carvedilol; Drug Therapy, Combination; Echocardiography; Female; Furosemide; Heart Function Tests; Hong Kong; Humans; Male; Predictive Value of Tests; Prognosis; Propanolamines; Ramipril; Spironolactone; Survival Rate; Tenascin; Tetrazoles; Turkey; Ventricular Remodeling

Anthracycline chemotherapy in cancer can cause severe, frequently fatal congestive heart failure (CHF), the first-line treatment for which is diuretics and digoxin. We have studied the use of an angiotensin-converting-enzyme (ACE) inhibitor added as a third agent.. In an observational study in hospital and as outpatients, 92 patients with advanced breast cancer were treated with epirubicin at a cumulative dose of 360 to 1000 mg/m2 (median 1000). Of 85 evaluable, nine developed life-threatening CHF at 1.5 to 13 months after ending epirubicin. Left ventricular ejection fraction (LVEF) decreased from normal to 18 to 35%. All received frusemide and digoxin, and then, after transient clinical relief, enalapril or ramipril (initially 1.25 mg orally daily, increasing to 10-15 mg after 4-6 weeks).. Eight of the nine patients deteriorated while on digoxin/diuretic. Within 3 months of starting the ACE inhibitor in these patients, LVEF had increased to normal or near normal. Only one patient died in heart failure. Follow-up ranged from 11 to 42 months (median 26). The ACE inhibitor was well-tolerated, with no first-dose hypotension, except for one patient who discontinued treatment after 6 months because of persistent cough. Two others discontinued treatment with their ACE inhibitor after 22 and 28 months because they felt well. Survival in the nine patients was similar to that of those who did not develop CHF.. Our experience suggests that treatment of anthracycline-induced CHF with an ACE inhibitor should start soon after clinical improvement on digoxin/diuretic regardless of the severity of symptoms rather than waiting for clinical deterioration.

Topics: Adult; Angiotensin-Converting Enzyme Inhibitors; Antibiotics, Antineoplastic; Breast Neoplasms; Cardiomyopathy, Dilated; Enalapril; Epirubicin; Female; Humans; Middle Aged; Prospective Studies; Ramipril; Stroke Volume; Treatment Outcome; Ventricular Function, Left

The objectives of this article are to determine the possible mechanism of functional mitral regurgitation in patients with dilated cardiomyopathy (DCM) and to know the effect of ramipril on left ventricle (LV) and mitral regurgitation by ECHO. Several postulates are put forth for functional mitral regurgitation in DCM, and mitral annular dilatation is said to be the primary mechanism in the past, but the exact mechanism is not clear. Though angiotensin converting enzyme (ACE) inhibitors are known to remodel the LV, their beneficial effect in patients with DCM with functional mitral regurgitation is not known. Various cardiac dimensions and degree of mitral regurgitation were measured by echocardiography in 30 normal control group and in 30 patients with DCM of various etiologies except ischemic, before and after ramipril therapy. There was a significant difference in all parameters especially sphericity of left ventricle and position of papillary muscles (P < 0.0003) in DCM patients, but mitral valve annulus did not show significant change (P < 0.3) compared to control group. In 50% of the patients, the functional mitral regurgitation totally disappeared. In 30% of patients, it came down from grade II to I or became trivial. In 20% of patients, it remained unchanged. There was remarkable improvement in sphericity, LV dimension, volumes, and EF%, which increased from 31 +/- 9.81 to 39.3 +/- 8.3% (P < 0.0003). It is concluded that echocardiography clearly demonstrates the increased sphericity of LV in DCM. The lateral migration of papillary muscles possibly plays a major role in functional mitral regurgitation. Ramipril significantly reduces not only sphericity but also functional mitral regurgitation.

Topics: Adolescent; Adult; Aged; Angiotensin-Converting Enzyme Inhibitors; Cardiomyopathy, Dilated; Case-Control Studies; Child; Echocardiography, Doppler, Color; Female; Follow-Up Studies; Heart Function Tests; Hemodynamics; Humans; Male; Middle Aged; Mitral Valve Insufficiency; Probability; Prospective Studies; Ramipril; Reference Values; Risk Assessment; Sensitivity and Specificity; Severity of Illness Index; Stroke Volume; Treatment Outcome; Ventricular Function, Left

A 32-year-old competitive soccer player presented with palpitations he had felt for 4 weeks during maximal activity (soccer training and match). The physical examination and an exercise electrocardiogram were carried out by his general practitioner up to 19 s at 350 W and a heart rate of 147/min without showing any abnormalities.. All blood parameters revealed no signs of illness. During treadmill exercise at a heart rate of 181/min, a non-sustained ventricular tachycardia was induced. Echocardiography showed a dilated left ventricle with an enddiastolic diameter of 70 mm and low fractional shortening (28 %). Cardiac catheterization demonstrated a diminished left ventricular ejection fraction (38 %) and an enlarged enddiastolic volume (199 ml) without signs of coronary artery disease. Electrophysiologic testing induced a non-sustained ventricular tachycardia.. The echocardiographic and angiographic results indicated a dilated cardiomyopathy. Competitive sports activities were stopped and treatment with a beta-blocker (metoprolol) and an ACE-antagonist (ramipril) was started.. In young male and female athletes, the possibility of severe cardiac abnormalities have to be considered even in the presence of good physical fitness and performance. To reach a high sensitivity for diagnostic ergometry, the work-load must reach the maximal capacity of the cardio-pulmonary system. Differences in the exercise performance of athletes and untrained subjects have to be considered.

Topics: Adrenergic beta-Antagonists; Adult; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Antihypertensive Agents; Cardiac Catheterization; Cardiomyopathy, Dilated; Echocardiography, Doppler, Color; Electrocardiography; Exercise Test; Heart Rate; Humans; Male; Metoprolol; Ramipril; Sensitivity and Specificity; Soccer; Stroke Volume; Tachycardia, Ventricular

Sustained or chronic tachyarrhythmia can produce reversible changes of atria or/and ventricles that induce systolic or/and diastolic disfunction, dilatation of heart chambers and progressive symptoms of heart failure. The changes regress after restoration of sinus rhythm. This is the clinical case, when at the beginning of the treatment, primary dilated cardiomyopathy is diagnosed to the patient having chronic atrial fibrillation and later after restoration of sinus rhythm and subsequent reduction of heart chambers as well as improvement of systolic function, past changes was assessed as reversible arrhythmogenic cardiomyopathy.

Topics: Adult; Amiodarone; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Anticoagulants; Antihypertensive Agents; Atrial Fibrillation; Cardiomyopathy, Dilated; Echocardiography; Electric Countershock; Electrocardiography; Follow-Up Studies; Humans; Male; Ramipril; Time Factors; Warfarin

Because part of the cardioprotective effects of angiotensin-converting enzyme (ACE) inhibitors results from their protective effects on cardiac bradykinin (BK) metabolism, the purpose of this study was to define the metabolism of BK in normal and failing human hearts and to compare the effect of omapatrilat, a vasopeptidase inhibitor (VPI), which simultaneously inhibits both neutral endopeptidase (NEP) and ACE, with that of an ACE inhibitor. Exogenous BK at a nanomolar concentration was incubated alone, in the presence of an ACE inhibitor (ramiprilat, 36 nM), or in the presence of a VPI (omapatrilat, 61 nM) with left ventricular membranes prepared from normal donor hearts (n = 7), and hearts from patients with an ischemic (n = 11) or dilated (n = 12) cardiomyopathy (DCM). The half-lives calculated for BK alone (199 +/- 60, 224 +/- 108, and 283 +/- 122 s; P = NS) exhibited similar values for normal, ischemic, and DCM heart tissues, respectively. Ramiprilat significantly increased the half-life of BK (P <.01), but the effect was similar for the three kinds of tissues (297 +/- 104, 267 +/- 157, and 407 +/- 146 s, respectively; P = NS). The potentiating effect of the VPI omapatrilat on the kinetic parameter of BK (478 +/- 210, 544 +/- 249, and 811 +/- 349 s, respectively) was greater than that of the ACE inhibitor (P <.01). Moreover, omapatrilat had a more important potentiating effect with DCM than normal heart membranes (P <.05). These results show that not only ACE but also and mainly NEP play an important role in the degradation of BK in human heart membranes. Omapatrilat, a VPI, has a greater protective effect on BK metabolism than that of a pure ACE inhibitor. Thus, inhibition of both ACE and NEP with omapatrilat could be more cardioprotective than ACE inhibition alone.

Topics: Angiotensin-Converting Enzyme Inhibitors; Bradykinin; Cardiomyopathy, Dilated; Cardiovascular Agents; Female; Half-Life; Heart; Humans; Male; Membranes; Middle Aged; Myocardial Ischemia; Myocardium; Neprilysin; Peptidyl-Dipeptidase A; Protease Inhibitors; Pyridines; Ramipril; Thiazepines

Topics: Cardiomyopathy, Dilated; Chronic Disease; Digoxin; Diuretics; Drug Evaluation; Drug Therapy, Combination; Exercise Tolerance; Heart Failure; Hemodynamics; Humans; Middle Aged; Ramipril; Rheumatic Heart Disease; Time Factors

Although a major goal in the treatment of chronic heart failure is to improve daily physical activity levels, this has not been assessed quantitatively. An increased daily activity level may be reflected by an increase in daily energy expenditure. In the present study, measurements of energy expenditure with a commercially available ambulatory calorimeter were first validated using cardio-pulmonary exercise tests in 5 normal volunteers. The energy expenditure measured by the calorimeter correlated well with that estimated from oxygen uptake (r = 0.89). Subsequently, the daily energy expenditure was serially measured with the calorimeter during long-term administration of the converting enzyme inhibitor ramipril for 24 weeks in 8 patients with chronic heart failure. Changes in echocardiographic parameters and exercise capacity were also studied. Peak oxygen uptake and anaerobic threshold assessed with symptom-limited maximal bicycle exercise were significantly increased 12 weeks or more after the initiation of treatment (P < 0.01 and P < 0.01, respectively). Left ventricular fractional shortening substantially, but not significantly, increased during this period (P < 0.1). These results strongly suggest that an overall improvement in heart failure was achieved after long-term ramipril therapy. The energy expenditure during daily activities was also significantly increased after ramipril therapy for 24 weeks (P < 0.01). Thus, the daily energy expenditure increased with improvement of heart failure, probably reflecting an increase in daily activity levels. We conclude that calorimetric measurement of daily energy expenditure is a novel and simple technique for quantitative evaluation of the effect of therapy on daily physical activity levels in patients with chronic heart failure.

Topics: Activities of Daily Living; Adult; Aged; Angiotensin-Converting Enzyme Inhibitors; Calorimetry; Cardiomyopathy, Dilated; Drug Therapy, Combination; Echocardiography; Energy Metabolism; Evaluation Studies as Topic; Exercise Test; Heart Failure; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Oxygen Consumption; Physical Exertion; Ramipril; Vasodilator Agents; Ventricular Function, Left