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PubMed1998

Effects of dichloroacetate in patients with congestive heart failure.

BACKGROUND: Conventional approaches to management of congestive heart failure (CHF) rely on drugs that increase myocardial contractility or reduce ventricular afterload. These approaches often improve cardiac symptoms and survival, but may be associated with significant deleterious effects. An alternative approach is to enhance myocardial energy production. Dichloroacetate (DCA) stimulates pyruvate dehydrogenase activity and accelerates aerobic glucose, pyruvate, and lactate metabolism in myocardial cells. These alterations would be expected to improve myocardial function. HYPOTHESIS: The purpose of the investigation was to assess the efficacy of DCA in patients with left ventricular systolic dysfunction and to examine the mechanism by which improvement occurs. METHODS: A total of 25 patients (16 men, 9 women; age range 31-72 years, mean 59) with CHF and ejection fraction < or = 40% received an intravenous infusion of 50 mg/kg DCA over 15 min. Indices of systolic and diastolic function were obtained by two-dimensional and Doppler echocardiography performed at baseline, 30 min, and 60 min following completion of DCA infusion. RESULTS: Baseline ventricular ejection fraction was 27.3 +/- 9.1%; 17 patients (68%) had nonischemic cardiomyopathy. Heart rate increased after DCA infusion from 73.9 +/- 14.5 to 79.2 +/- 14.9 beats/min at 60 min; p = 0.02. Left ventricular diastolic and systolic volumes increased at 30 min compared with baseline (248.7 +/- 98.1 vs. 259.6 +/- 99.6; p = 0.04, and 180.1 +/- 80.4 vs. 192.2 +/- 84.9; p = 0.002, respectively), but stroke volume (49.2 +/- 19.1 vs. 48.9 +/- 18.1; p = 0.9) and ejection fraction (27.3 +/- 9.1 vs. 25.7 +/- 9.8; p = 0.2) were unchanged. Indices of diastolic function were also unchanged. CONCLUSION: Dichloroacetate infusion in patients with CHF is not associated with improvement in noninvasively assessed left ventricular function.

Adult↗
PubMed2005

Transcardiac gradients of N-terminal B-type natriuretic peptide in aortic valve stenosis.

BACKGROUND: Plasma B-type natriuretic peptide (BNP), as well as the N-terminal part of the prohormone (Nt-BNP), are frequently elevated in aortic valve stenosis (AS). Yet, their release from the heart into the circulation has never been directly studied in AS. AIM: To assess the release of Nt-BNP in AS with focus on the identification of its main determinants. METHODS: We studied 49 adult patients undergoing preoperative cardiac catheterization for isolated AS. Blood was sampled from the aortic root and the coronary sinus for Nt-BNP determination by immunoassay. RESULTS: The mean (+/-S.E.) transcardiac Nt-BNP step-up averaged 79+/-53 pmol/l in 11 control patients free of structural heart disease, 75+/-32 pmol/l in 31 AS patients free of heart failure (HF), 236+/-62 pmol/l in 8 AS patients with diastolic HF (ejection fraction > or = 50%, pulmonary wedge pressure > 14 mm Hg) and 469+/-66 pmol/l in 7 AS patients with systolic HF (ejection fraction < 50%, wedge pressure > 14 mm Hg) (p<0.001). The transcardiac Nt-BNP gradient was independently associated with left ventricular (LV) end-diastolic pressure (beta=0.47, p<0.001) and ejection fraction (beta=-0.29, p<0.019) and with co-existent coronary artery disease (beta=0.23, p=0.050). CONCLUSION: LV diastolic and systolic dysfunction along with coronary artery disease are likely to be the key determinants of cardiac Nt-BNP release in AS. The transcardiac Nt-BNP gradient increases on average three-fold with the development of diastolic HF and six-fold in systolic HF.

Aged↗
PubMed2006

Echocardiographic study of cardiac morphological and functional changes before and after parturition in pregnancy-induced hypertension.

PURPOSE: To investigate the cardiac morphological and functional changes by echocardiography, before and after parturition in patients with pregnancy-induced hypertension (PIH). METHODS: The parameters related to cardiac morphology and left ventricular diastolic and systolic functions were compared before and after parturition in 32 patients with PIH and 24 normal pregnant (NP) women. RESULTS: Compared with NP women, the PIH patients had greater diameters of left atrium and left ventricle in end-diastole (LAd: 38.9 +/- 4.5 vs 34.6 +/- 4.4 mm, P = 0.0015; LVEDd: 51.2 +/- 5.8 vs 47.1 +/- 4.2 mm, P = 0.036) and lower E/A (1.2 +/- 0.2 vs 1.4 +/- 0.2, P = 0.009) and greater fractional shortening (FS) (39.8 +/- 6.5% vs 37.1 +/- 6.9%, P = 0.042) and ejection fraction (EF) (0.72 +/- 0.07 vs 0.66 +/- 0.08, P = 0.040). Pericardial effusion (PE) occurred in 31.3% and 16.7% of PIH and NP, respectively. The LAd and LVEDd in 70% and 47% patients with PIH resolved and PE disappeared in 80% of PIH patients postpartum. E/A ratio in PIH significantly increased after parturition, while the two patients with cardiac systolic dysfunction did not improve very much. CONCLUSIONS: Compared with normal pregnancy, the most significant cardiac morphological changes in PIH are the greater diameters of left atrium and left ventricle, thicker inter-ventricular septum (IVS), more PE, impaired left ventricular diastolic function, and increased systolic function. The PE could disappear in PIH and about half of other abnormalities could recover to be the level of normal pregnancy postpartum within 2 months.

Adult↗
PubMed1992

[Relationship between left ventricular systolic function and the myocardial gray level distribution in patients with idiopathic dilated cardiomyopathy].

Dilated cardiomyopathy (DCM) is characterized by progressive left ventricular (LV) systolic dysfunction of nonspecific etiology. Fifty-nine DCM patients were serially observed by echocardiography for 4.5 +/- 2.6 years, and 7.3 +/- 3.4 times M-mode and two-dimensional echocardiography was performed during the observation period using SSH-11A (Toshiba). To assess LV systolic function, ejection fraction was calculated by Pombo's method. Myocardial gray level distribution shown by echocardiography was calculated to assess the myocardial tissue character. Two-dimensional echocardiographic images were obtained in the parasternal short-axis view, recorded on U-matic videotape, and transferred to an image processing computer system (MIPRON, Kontron). The images were digitized and stored on the computer. The regions of interest (ROI) were placed in the LV septum, posterior papillary muscle, posterior wall, anterior papillary muscle and entire LV wall. The gray level distributions in each ROI and its quantitative parameters (mean, SD, skewness, excess) were calculated. The corrected myocardial gray level of every ROI (CMD) was also calculated and expressed as the ratio to the mean gray level of the LV cavity. Seven patients exhibited significant decreases in ejection fraction (more than 10%) during the observation period (group A); the remainders showed less change (group B).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomyopathy, Dilated↗
PubMed2003

Use of strain imaging in detecting segmental dysfunction in patients with hypertrophic cardiomyopathy.

BACKGROUND: The distribution and magnitude of left ventricular hypertrophy are not uniform in patients with hypertrophic cardiomyopathy (HCM). Previous echocardiographic studies have focused on global left ventricular function. Recently, myocardial Doppler strain (epsilon) imaging, a newly developed technique, has allowed the quantification of regional myocardial motion. The aim of this study was to characterize regional left ventricular systolic function by myocardial Doppler epsilon imaging in patients with HCM. METHODS: Included in this study were 31 patients with asymmetric septal hypertrophy and HCM, and 41 age-matched healthy patients. Regional longitudinal axial systolic epsilon was assessed at the basal, mid, and apical segments of the septal and lateral walls and compared between both groups. RESULTS: Patients with HCM had reduced epsilon at the ventricular septum (-10.3 +/- 5.7%) compared with control patients (-19.4 +/- 3.3%, P <.001). In the HCM group, epsilon in the midseptum (-1.3 +/- 8.2%) was significantly less than at the basal (-12.2 +/- 8.7%, P <.01) and apical septum (-17.3 +/- 10.4%, P <.01), and was also less than at the midlateral wall (-9.4 +/- 5.3%, P <.05). There was a significant correlation between midseptal epsilon and intraventricular septum to posterior wall thickness ratio (r = 0.81, P <.001). CONCLUSION: Midseptal longitudinal epsilon was markedly decreased, even reversed in patients with HCM (paradoxic longitudinal systolic expansion), which was directly related to the degree of septal hypertrophy. Myocardial Doppler epsilon imaging could offer a unique approach to quantify regional systolic dysfunction in these patients.

Adult↗
PubMed1999

[Clinical presentation and coronary angiographic results in unstable angina pectoris].

The syndrome "unstable angina" (UA) covers a broad spectrum of patients. In this study we tried to determine the relationship between the severity of UA and angiographic findings. We evaluated 1000 consecutive patients undergoing coronary angiography. Those with the clinical diagnosis "UA" were included in the study. In a retrospective analysis of their records we categorized them, using the Braunwald-classification for determination of the severity of the disease. 352 patients were include, 209 men and 143 women, the mean age was 65 years. 47% met Braunwald-Class I, 26% Class II and 27% Class III. Coronary single-vessel disease was present in 29%, two-vessel disease in 20%, three-vessel disease in 25%, normal coronaries in 13% and coronary atherosclerosis without critical narrowing in 13%. Left ventricular function was preserved in 72%, mild systolic dysfunction was found in 10%, moderate in 13% and severe in 5%. There was no overall correlation between clinical presentation (Braunwald-Classes) and angiographic findings. Women showed a similar distribution of Braunwald-Classes, but significantly more coronary arteries without critical obstruction. In patients with reduced systolic function the percentage of multi-vessel disease was significantly higher, the percentage without relevant coronary artery narrowing was significantly lower. 1) The lack of overall correlation between clinical presentation and angiographic findings supports the importance of coronary angiography in the evaluation of patients with UA. 2) The assessment of women with chest pain is more difficult than of men with regard to coronary heart disease. 3) UA in patients with impaired left ventricular function is a predictor of severe coronary artery disease.

Aged↗
PubMed2006

Myocardial dysfunction in polymyositis.

Myocardial involvement in polymyositis is occasionally suspected, but symptomatic cardiac dysfunction is rarely reported. Described in the present report is a 48-year-old woman with a two-year history of polymyositis who suddenly developed near fatal ventricular arrhythmia, and a 56-year-old man with a relapsing polymyositis who developed severe systolic dysfunction. These two cases emphasize the importance of systematic cardiac evaluation when the diagnosis of polymyositis is initially made and the necessity of re-evaluating cardiac function, even in the presence of clinical remission and normalization of creatine phosphokinase with treatment.

Cardiomyopathies↗
PubMed2004

Na+/H+ exchange inhibition attenuates left ventricular remodeling and preserves systolic function in pressure-overloaded hearts.

Cardiac hypertrophy is a homeostatic response to elevated afterload. Na+/H+ exchanger (NHE) inhibition reduces the hypertrophic response in animal models of left ventricular hypertrophy (LVH) and myocardial infarction. We examined the effect of chronic treatment with cariporide, a selective inhibitor of Na+/H+ exchanger isoform 1 (NHE-1), on left ventricular (LV) systolic and diastolic function under pressure overload conditions. Male CD-1 mice were randomized to receive either a control diet or an identical diet supplemented with 6000 p.p.m. of cariporide. Cardiac pressure overload was induced by thoracic aortic banding. LV dimension and systolic and diastolic function were assessed in sham and banded mice by echocardiography and cardiac catheterization 2 and 5 weeks after surgery. Histological analysis was also performed. After 2 weeks of pressure overload, the vehicle-treated banded mice (Veh-Bd) had enhanced normalized LV weight (about +50%) and normal chamber size and function, whereas cariporide-treated banded mice (Car-Bd) showed a preserved contractility and systolic function despite a marked attenuation of LVH. Diastolic function did not differ significantly among groups. After 5 weeks, the Veh-Bd developed LV chamber enlargement and systolic dysfunction as evidenced by a 16% increase in LV end-diastolic diameter, a 36% decrease in myocardial contractility, and a 26% reduction in percent fractional shortening. In contrast, Car-Bd showed an attenuated increase in LV mass, normal chamber size, and a maintained systolic function. A distinct histological feature was that in banded mice, cariporide attenuated the development of cardiomyocyte hypertrophy but not the attendant myocardial fibrosis. In conclusion, the results of the present study indicate that (i) the hypertrophic response to pressure overload is dependent on NHE-1 activity, and (ii) at the 5-week stage, banding-induced deterioration of LV performance is prevented by NHE-1 inhibition.British Journal of Pharmacology (2004) 141, 526-532. doi:10.1038/sj.bjp.0705631

Animals↗
PubMed1986

Diastolic filling dynamics in patients with aortic stenosis.

Left ventricular filling dynamics were investigated in 24 patients with aortic stenosis (AS). Biplane cineangiography was performed with simultaneous micromanometry in these 24 patients and in six control subjects. Twelve of the patients with AS had moderate hypertrophy with a left ventricular muscle mass index of less than 180 g/m2 (ASI group) and 12 had severe hypertrophy with an index of 180 g/m2 or more (AS2 group). Filling dynamics were also evaluated postoperatively in eight patients in the AS1 and six patients in the AS2 group. Preoperatively, end-diastolic and end-systolic volume indexes were larger and ejection fraction was lower in the AS2 compared with the control or AS1 group. Percent volume increase during the first half of diastole (%V1) was smaller in the AS1 than in the AS2 group. Peak filling rate in the first half of diastole (PFR 1) was higher in the AS2 than in the control or in AS1 group, while peak filling rate in the second half of diastole (PFR2) was considerably greater in the AS1 group than in the other two groups. The time constant of left ventricular pressure decline, an index of the rate of relaxation, was prolonged in the AS2 group. In contrast, mitral valve opening pressure (MVOP) was significantly higher in this group than in the other two groups. The constant of left ventricular chamber stiffness was slightly but not significantly greater in both AS groups than in the control subjects. After surgery in patients in the AS1 group, preoperatively reduced %V1 had increased and preoperatively enhanced PFR2 had decreased. In patients in the AS2 group, excluding one with a persistent low ejection fraction after surgery, preoperatively enhanced PFR1 decreased in association with a decrease in MVOP. Thus, left ventricular filling dynamics vary in patients with AS depending on the degree of left ventricular hypertrophy and systolic function. In patients with AS and moderate hypertrophy %V1 is slightly reduced but is compensated for by a forceful atrial contraction. In those with severe hypertrophy and systolic dysfunction increased driving pressure allows %V1 to remain within normal limits, despite prolonged left ventricular relaxation and decreased elastic recoil. Both changes in left ventricular filling dynamics tend to normalize after surgery in association with a reduction in left ventricular hypertrophy and/or an improvement of systolic function.

Adult↗
PubMed2003

[Hypertensive heart disease and microangiopathy].

Cardiac alterations in patients with arterial hypertension comprise the manifestation of stenosis in epicardial arteries, disease of coronary resistive vessels, prothrombotic changes and endothelial dysfunction, pronounced perivascular and interstitial fibrosis, left ventricular hypertrophy, dilatation of the left atrium, increased sympathetic drive and degeneration of aortic valve. These alterations leads to the major clinical manifestations of hypertensive heart disease, that are symptoms of reduced coronary conductance, left ventricular hypertrophy, diastolic and systolic dysfunction with or without left ventricular enlargement and arrhythmia. Different non-invasive and invase procedures are available for screening and follow up of patients with hypertensive heart disease. The primary therapeutic target is, apart from lowering blood pressure, to reverse cardiac manifestations of arterial hypertension using specific therapeutic algorithms.

Antihypertensive Agents↗
PubMed2002

Cardiac structure and function in young and senescent mice heterozygous for a connexin43 null mutation.

Downregulation of connexin43 (Cx43) in the failing heart has been implicated not only in arrhythmogenesis but in contractile dysfunction as well. Cx43-deficient mice exhibit reduced baseline conduction velocity and increased arrhythmias in response to ischemia. However, it is not known whether Cx43-deficient mice have any abnormalities in contractile function or, furthermore, whether cardiac dysfunction may be manifested in Cx43-deficient mice with advancing age. Therefore, we analyzed echocardiographic images from young and senescent Cx43-deficient C57BL/6Jx129 mice compared to wild-type littermate controls. Only a few, modest genotype-related differences were observed. LV wall thickness during systole and % fractional shortening were diminished by 8-10% in Cx43-deficient v wild-type mice. Aging alone had a greater effect on cardiac structure and function. LV mass and relative wall thickness were significantly increased in senescent v young mice independent of genotype. Percent fractional shortening and LV internal chamber dimension were significantly reduced in senescent v young mice. Thus, aging in mice, as in humans, is associated with concentric remodeling, mild systolic dysfunction and fibrosis. Although diminished Cx43 expression could contribute to contractile dysfunction in patients with advanced heart failure, genetic deficiency in Cx43 does not appear significantly to alter cardiac structure or function even in aged mice.

Aging↗
PubMedDate not supplied

[Impact of left ventricular patterns and diastolic dysfunction on hemodialysis patients].

BACKGROUND: Left ventricular hypertrophy is the main manifestation of uraemic cardiomyopathy and predicts both cardiovascular events and death independently of conventional risk factors. Diastolic dysfunction is often associated with left ventricular hypertrophy, and accounts for up to 30% of heart failure. The aim of this study was to estimate the impact and the prevalence of left ventricular hypertrophy, its geometric models and diastolic dysfunction on haemodialysis patients, as well as the relationship with cardiac troponin, a specific marker for myocardial damage. METHODS: We enrolled in the study 31 patients (26 on haemodialysis, 5 on peritoneal dialysis) and 31 normal healthy subjects as the control group. Echocardiographic measurements were carried out according to the recommendations of the American Society of Echocardiography. Left ventricular mass was calculated according to the Devereux formula and indexed to height 2.7 We carried out Doppler echocardiography to study the diastolic function by measurements of isovolumic relaxation period (IVRT), E-wave deceleration time (DTE) and E/A ratio. We measured cardiac troponin using a third generation electrochemiluminescence immunoassay. We did the statistical analysis with the t test for comparison among groups, and we established correlations using the Pearson and Spearman correlation test. We considered values of p<0.05 to be statistically significant. RESULTS: Eccentric hypertrophy was the most frequent pattern (n=17; 55%), followed by normal cardiac geometry (n=7; 23%) and concentric hypertrophy (n=5; 16%). Only a minority of patients (n=2; 6%) showed concentric remodelling. Systolic dysfunction was present in 3 patients (EF<50%). Diastolic dysfunction was present in 24 out of 31 HD patients, that had abnormal relaxation pattern, characterised by prolonged IVRT, prolonged DTE and E/A ratio <1. Only one patient had restrictive filling pattern with reduced DTE and E/A ratio >2. Fourteen patients (45%) had E/A ratio < or =0.5, 10 patients (32%) had E/A ratio >0.5<1 and 7 patients (13%) had E/A ratio > or =1. DTE was prolonged in 14 patients (45%) and IVRT was prolonged in 6 patients (19%). The patients with E/A ratio < or =0.5 (n=14; 45%) suffered major hypotensive episodes during dialytic sessions compared to patients with E/A ratio >0.5, we found this difference to be statistically significant (p < 0.01). We observed the E/A ratio to be negatively correlated with age (r = -0.41; p=0.02) whereas DTE was positively correlated with posterior wall thickness (r =0.36; p= 0.05) and interventricular septum thickness (r =0.45; p=0.01). Cardiac troponin was positively correlated with age (r =0.50; p=0.00), left ventricular mass (r =0.41; p=0.02), posterior wall thickness (r =0.41; p=0.02) and interventricular septum thickness (r =0.39; p=0.03) but not with diastolic dysfunction parameters. Serum cardiac troponin was elevated (> or =0.10 micro g/L) in 12 patients (38.7%) and was associated with eccentric hypertrophy in all the cases. We detected no significant differences among groups with normal left ventricular geometry and left ventricular hypertrophy in the duration of the dialytic treatment, but we noted a statistically significant difference in relationship to age (p=0.03). CONCLUSIONS: Left ventricular hypertrophy is associated with diastolic dysfunction, both cause of hypotensive episodes during dialytic treatments and heart failure in patients with normal systolic function. The non invasive assessment of left ventricular diastolic function would represent an important advancement in the diagnosis and prevention of heart failure in haemodialysis patients.

Diastole↗
PubMed2006

The effect of acute hypertension on left ventricular diastolic pressures in a canine model of left ventricular dysfunction with a preserved ejection fraction and elevated left ventricular filling pressures.

BACKGROUND: Decompensated heart failure with preserved left ventricular (LV) ejection fraction (EF) is often accompanied by hypertensive episodes. We hypothesized that acute increase in arterial pressure results in elevated early and late diastolic LV pressures as a result of further impaired LV relaxation. METHODS: To test this hypothesis, we used a chronic canine model of LV systolic dysfunction with preserved LV function (LVDPEF) (EF > 50%) and elevated LV end-diastolic pressure using coronary microsphere embolization. At baseline and with LVDPEF, each dog was paced 10 beats above their baseline heart rate and high-fidelity LV pressures, echocardiographic LV volumes, and transmitral Doppler were obtained before and after methoxamine pressure loading. RESULTS: With normal LV function, LV pressures at peak negative dP/dt (+18 mm Hg, P < .05) and at LV pressure minimum (+3.6 mm Hg, P < .01) increased. Both tau (P < .05) and LV end-diastolic pressure increased (5 +/- 3 vs 13 +/- 4 mm Hg, P < .01). EF was unchanged, although LV end-diastolic volume increased (P < .01). Pressure loading with LVDPEF resulted in a timing delay (P < .05) and a greater increase in LV pressures at peak negative dP/dt (+45 mm Hg) and LV minimal pressure (+7.5 mm Hg) as compared with normal LV function (P < .01). LV end-diastolic pressure increased (9 +/- 2-23 +/- 5 mm Hg, P < .001), diastolic filling period shortened (288 +/- 51-204 +/- 54 milliseconds, P < .01), and tau increased (P < .001). EF declined from 54 +/- 9% to 43 +/- 9% (P < .05) and LV size increased (P < .01). CONCLUSIONS: Pressure loading with normal LV function and with LVDPEF results in increased LV diastolic pressures, which are further exaggerated with LVDPEF as a result of prolonged relaxation and shortened diastolic filling.

Acute Disease↗
PubMed1995

A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group.

BACKGROUND: Treatment with angiotensin-converting-enzyme (ACE) inhibitors reduces mortality among survivors of acute myocardial infarction, but whether to use ACE inhibitors in all patients or only in selected patients is uncertain. METHODS: We screened 6676 consecutive patients with 7001 myocardial infarctions confirmed by enzyme studies. A total of 2606 patients had echocardiographic evidence of left ventricular systolic dysfunction (ejection fraction, < or = 35 percent). On days 3 to 7 after infarction, 1749 patients were randomly assigned to receive oral trandolapril (876 patients) or placebo (873 patients). The duration of follow-up was 24 to 50 months. RESULTS: During the study period, 304 patients (34.7 percent) in the trandolapril group died, as compared with 369 (42.3 percent) in the placebo group (P = 0.001). The relative risk of death in the trandolapril group, as compared with the placebo group, was 0.78 (95 percent confidence interval, 0.67 to 0.91). Trandolapril also reduced the risk of death from cardiovascular causes (relative risk, 0.75; 95 percent confidence interval, 0.63 to 0.89; P = 0.001) and sudden death (relative risk, 0.76; 95 percent confidence interval, 0.59 to 0.98; P = 0.03). Progression to severe heart failure was less frequent in the trandolapril group (relative risk, 0.71; 95 percent confidence interval, 0.56 to 0.89; P = 0.003). In contrast, the risk of recurrent myocardial infarction (fatal or nonfatal) was not significantly reduced (relative risk, 0.86; 95 percent confidence interval, 0.66 to 1.13; P = 0.29). CONCLUSIONS: Long-term treatment with trandolapril in patients with reduced left ventricular function soon after myocardial infarction significantly reduced the risk of overall mortality, mortality from cardiovascular causes, sudden death, and the development of severe heart failure. That mortality was reduced in a randomized study enrolling 25 percent of consecutive patients screened should encourage the selective use of ACE inhibition after myocardial infarction.

Adult↗
PubMed2004

Use of Beta Blockers in Patients with Post-MI Left Ventricular Dysfunction.

beta Blockers have been shown to reduce mortality after myocardial infarction (MI) in several large trials. Despite strong evidence supporting the role of beta blockers in treating patients after MI, less than half are prescribed these drugs. The majority of studies demonstrating efficacy of beta blockers in the treatment of the post-MI patients were conducted at a point in time when left ventricular (LV) dysfunction was considered a strong contraindication to their use. In addition, when these studies were carried out a variety of therapies that are known to improve survival were not yet available. In the present era, beta blockers are routinely used to treat patients with heart failure due to systolic dysfunction. Until recently, however, there was uncertainty about their role in the management of patients with LV dysfunction after MI. The recent CAPRICORN (Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction) study demonstrated a significant mortality benefit when carvedilol was added to standard therapy in patients with LV dysfunction after MI. This article reviews information regarding the initiation and maintenance of beta blockers in patients with post-MI LV dysfunction.

Journal Article↗
PubMed2002

A case of reversible dilated cardiomyopathy after alpha-interferon therapy in a patient with renal cell carcinoma.

A 47-year-old man with renal cell carcinoma underwent nephrectomy, and postoperative chemotherapy was performed with recombinant alpha-interferon. Five years later, he experienced dyspnea during physical exertion. An echocardiogram revealed dilatation and systolic dysfunction of the left ventricle, and thallium-201 myocardial scintigraphy showed diffuse heterogeneous perfusion. We diagnosed congestive heart failure because of cardiomyopathy induced by alpha-interferon therapy. Withdrawal of interferon therapy and the combination of an angiotensin-converting enzyme inhibitor, diuretics, and digitalis improved left ventricular systolic function. Furthermore, myocardial scintigraphy using [123I] beta-methyl-p-iodophenylpentadecanoic acid (123I-BMIPP) or [123 I]metaiodobenzylguanidine (123I-MIBG) revealed normal perfusion after the improvement of congestive heart failure. This is a rare case of interferon-induced cardiomyopathy that resulted in normal myocardial images in 123I-BMIPP and 123I-MIBG scintigrams after withdrawal of interferon therapy.

Antineoplastic Agents↗
PubMed1998

Should we screen for asymptomatic left ventricular dysfunction to prevent heart failure?

A programme to detect and treat asymptomatic left ventricular dysfunction would seem to fulfil all five principles of screening. Indeed, such a programme would appear to be at least as firmly based as those already in existence for, for example, cervical and breast cancer. Further evaluation of the screening of high risk groups to detect asymptomatic left ventricular systolic dysfunction with the aim of giving treatment to prevent the development of heart failure is merited.

Clinical Trials as Topic↗
PubMedDate not supplied

An ovine model of chronic heart failure: echocardiographic and tissue Doppler imaging characterization.

BACKGROUND AND AIM OF THE STUDY: Heart failure in the western world is a major health-care issue. In order to validate novel surgical or pharmacological treatments, reproducible animal models of left ventricular dysfunction are necessary. In the current study, we report our data and experience with a model of toxin-induced heart failure in the sheep. METHODS: Sequential intracoronary injections of doxorubicin (0.75 mg/kg) were carried out every 2 weeks until standard echocardiographic and tissue Doppler imaging detection of myocardial systolic dysfunction. The animals were assessed 1 month later and harvested. Indices of cardiac function from baseline to last day of protocol were recorded and their differences were evaluated by a Wilcoxon rank test for paired data. RESULTS: Ten sheep received 2.5 +/- 0.7 intracoronary injections of a cumulative dose of 88.8 +/- 25 mg/m2 doxorubicin. All available parameters demonstrated signs of severe cardiac dysfunction with statistical significance. All hearts demonstrated severe histological lesions, some of which were consistent with doxorubicin-induced toxicity. CONCLUSIONS: The present study shows that this ovine model is reproducible and stable. It can therefore be relevant to the study of chronic heart failure. It will be incorporated in our future studies concerning novel treatments (such as cell therapy) of nonischemic dilated cardiomyopathy.

Animals↗