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At least 127 records · Page 7Linked to original sources
PubMed1990

Left ventricular hypertrophy and impaired diastolic filling in essential hypertension. Diastolic mechanisms for systolic dysfunction during exercise.

Left ventricular ejection fraction is normal at rest but may respond abnormally to exercise in many patients with essential hypertension. To assess the determinants of the abnormal ejection fraction response to exercise, we performed radionuclide angiography at rest and during exercise in 41 hypertensive patients without coronary artery disease. In 22 patients (group 1), the ejection fraction increased more than 5% during exercise; in the other 19 patients (group 2), the ejection fraction either increased by less than 5% or decreased with exercise. Left ventricular diastolic filling was impaired at rest in patients in group 2 compared with group 1, with reduced peak filling rate (2.5 +/- 0.4 vs. 3.1 +/- 0.7 end-diastolic volume/sec; p less than 0.01) and prolonged time to peak filling rate (175 +/- 28 vs. 153 +/- 22 msec; p less than 0.01). Impaired diastolic filling in group 2 was associated with less augmentation in end-diastolic volume during exercise compared with group 1 (p less than 0.01). These observations were not dependent on the threshold value that was arbitrarily chosen to define an abnormal ejection fraction response, as there were significant correlations for the entire group between the magnitude of change in ejection fraction with exercise and both the resting peak filling rate (r = 0.46) and the change in end-diastolic volume with exercise (r = 0.62).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1997

A case of dilated cardiomyopathy with abnormal atrioventricular conduction 5 years before the appearance of left ventricular systolic dysfunction.

The first manifestation of dilated cardiomyopathy is usually dyspnea as a result of left heart failure. In this report we describe an unusual patient with third-degree atrioventricular (AV) block unaccompanied by left ventricular dysfunction. Severe left ventricular dysfunction occurred 5 years after the implantation of a permanent pacemaker. We conclude that AV block should not be overlooked as an initial clinical manifestation of dilated cardiomyopathy.

Adult↗
PubMed1994

Blockade of the renin-angiotensin system. Effect on mortality in patients with left ventricular systolic dysfunction.

Blockade of the renin-angiotensin-aldosterone system (RAAS) has been shown to be effective in reducing morbidity and mortality in patients with symptomatic left ventricular dysfunction. Angiotensin converting enzyme inhibitors (ACE-I) should be administered to all patients with symptomatic left ventricular dysfunction unless contraindicated or not tolerated. Although ACE-Is are effective, there is reason to believe that further blockade of the RAAS by aldosterone antagonists and/or alternative means of blocking the RAAS by use of renin inhibitors or angiotensin II receptor blocking agents may have an important role in the future. The finding in the SOLVD and SAVE trials that ACE-Is are effective in reducing recurrent ischemic events in patients with left ventricular dysfunction also holds great promise for the future, not only for patients with left ventricular dysfunction but also as a possible secondary prevention of ischemic heart disease in patients without left ventricular dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

[Is the treatment of left ventricular systolic dysfunction different according to the etiology?].

Cardiac failure is the terminal stage of evolution, the finality of many valvular, vascular, myocardial, general, congenital or acquired conditions. The therapeutic decisions should be based on the search for a curable cause of a predisposing factor and the evaluation of the severity of the cardiac failure. At advanced stages of ventricular dysfunction when the myocardial lesions are constituted, when cardiac and vascular remodelling has occurred, the aetiological treatment, which is the constant objective, is unfortunately too late. The treatment is the same, whatever the aetiology, in order to improve functional problems. At early stages, and, if possible, preventively, surgery, revascularisation techniques, the correction of an arrhythmia, the suppression of a cardiotoxic factor, are essential. The different therapeutic classes used could have different efficacies depending on the aetiology, but, finally, this point is negligible: the medications are based on the results of large scale, controlled, therapeutic trials.

Cardiovascular Surgical Procedures↗
PubMed1993

Obesity and the heart.

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increased total blood volume creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular (LV) hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The presence of systemic hypertension in obese individuals facilitates development of LV dilatation and hypertrophy. Congestive heart failure may occur in such individuals, and may be attributable to LV diastolic dysfunction or to combined LV diastolic and systolic dysfunction. The sleep apnea/obesity hypoventilation syndrome occurs in 5% of morbidly obese individuals and is potentially life-threatening. Treatment of obesity cardiomyopathy consists of weight loss, salt restriction, and diuretics. Digitalis and vasodilators may be useful in selected cases. Central obesity is probably a risk factor for the development of coronary heart disease. Alterations in lipid and insulin metabolism may facilitate development of coronary heart disease in obese patients.

Heart Diseases↗
PubMed1993

Role of mechanical and hormonal factors in cardiac remodeling and the biologic limits of myocardial adaptation.

Patients with chronic congestive heart failure manifest > or = 1 of the following abnormalities: diastolic dysfunction, systolic dysfunction, and arrhythmias. Diastolic dysfunction, one of the first symptoms to occur during hypertensive cardiopathy, depends on both active relaxation of the cardiac muscle and passive ventricular compliance. The ability of the ventricles to relax depends on normal calcium metabolism and adenosine triphosphate concentration. Ability to extrude intracellular calcium is depressed in the hypertrophied, overloaded heart as compared with the normal myocardium. Myocardial fibrosis is the major cause of increased diastolic ventricular stiffness. Left ventricular (LV) hypertrophy and myocardial fibrosis also greatly increase the likelihood of ventricular arrhythmias, in particular by prolonging the QRS interval and facilitating the occurrence of reentry arrhythmias. Findings in animal studies have indicated that such fibrosis, which involves excessive collagen deposition, is independent of LV hypertrophy and that LV hypertrophy does not necessarily result in myocardial fibrosis. Instead, the development of myocardial fibrosis is sensitive to circulating levels of both angiotensin II and aldosterone, and the fibrotic response to each of these substances is independent. The aldosterone antagonist spironolactone prevents myocardial fibrosis in several animal models, thus confirming the importance of aldosterone in the genesis of excessive collagen deposition.

Adaptation, Physiological↗
PubMed1995

Effects of lisinopril on congestive heart failure in normotensive patients with diastolic dysfunction but intact systolic function.

This study examined the effects of lisinopril on diastolic function in 12 normotensive patients (mean age 72 years) with symptomatic congestive heart failure, intact left ventricular systolic function and abnormal diastolic function secondary to ischaemic heart disease in a placebo-controlled double blind crossover study, with each treatment dosed orally for 5 continuous weeks. Compared to placebo, lisinopril significantly decreased blood pressure, increased plasma renin activity without altering heart rate or plasma norepinephrine. There was no statistically significant improvement with lisinopril in radionuclide derived peak filling rate and time to peak filling rate, in Doppler echocardiographic measurements of the ratio of peak flow velocity in early diastole to the peak flow velocity of atrial contraction (E:A ratio) and in visual analogue scales of symptoms. Thus, although angiotension converting enzyme inhibitors may have an established role in the treatment of heart failure secondary to left ventricular systolic dysfunction, its use in patients with isolated diastolic dysfunction remains unclear.

Aged↗
PubMed1994

Which left ventricular function is impaired earlier in the evolution of diabetic cardiomyopathy? An echocardiographic study of young type I diabetic patients.

OBJECTIVE: To determine whether diastolic dysfunction preceded systolic dysfunction in the evolution of diabetic cardiopathy. RESEARCH DESIGN AND METHODS: A total of 157 young (mean age 26.6 years) cardiac asymptomatic type I diabetic patients and 54 age- and sex-matched healthy (nondiabetic) subjects were studied. The severity of diabetic complications (retinopathy, nephropathy, and cardiac autonomic neuropathy) was evaluated by the diabetic complication index (DCI), a sum of individual scores for each complication. Left ventricular (LV) function was studied by M-mode echocardiography. Impaired systolic and diastolic functions were presumed if at least two echocardiographic variables for systolic function (fractional shortening [FS], mean velocity of circumference fiber shortening, and stroke index) and for diastolic function (slope of anterior mitral leaflet in early diastole, isovolumic relaxation time [IRT], and left atrium emptying index) were out of the control range (mean +/- 2 SD). RESULTS: Diastolic dysfunction was twice as common as systolic dysfunction (27% and 12%, respectively, P < 0.001). Of diabetic patients with systolic dysfunction, 83% had impaired diastolic function, whereas only 30% of diabetic patients with diastolic dysfunction had systolic damage (P < 0.001). On the other hand, only 3 of 157 diabetic patients (1.9%) had systolic dysfunction with preserved diastolic function (P > 0.05). Diastolic dysfunction, represented by the interval from minimal LV dimension to mitral valve opening, was seen in diabetic patients approximately 8 years after onset of diabetes and systolic dysfunction represented by FS after approximately 18 years. Diastolic dysfunction, represented by IRT, was found in the presence of mild complications (DCI = 2), and systolic dysfunction, represented by FS, was found in the presence of more severe complications (DCI = 4). CONCLUSIONS: Our findings indicate that myocardial damage in patients with diabetes affects diastolic function before systolic function. The intentional assessment of diastolic function is advisable for early detection of LV dysfunction before clinical symptoms appear, with follow-up to detect further deterioration of cardiac status.

Adult↗
PubMed1982

Systolic time intervals in the evaluation of thyroid dysfunction.

Systolic time intervals, the pre-ejection period (PEP), left ventricular ejection time (LVET) and PEP/LVET ratio were studied in ten thyrotoxic and ten hypothyroid patients. LVET and PEP intervals were corrected for heart rate (LVETc and PEPc). The measurements were repeated after 1-28 months when the patients were euthyroid following appropriate therapy. Compared with the euthyroid values, the PEPc intervals and PEP/LVET ratios were significantly decreased (p less than 0.01) in the thyrotoxic and increased (p less than 0.001) in the hypothyroid patients. In both groups the LVETc intervals were significantly prolonged (p less than 0.001). In four of the hypothyroid patients the PEP/LVET ratios were markedly increased (above 0.60, mean 0.66), and above 0.41 in the euthyroid state (reference value 0.35 +/- 0.05). In the other hypothyroid patients and in thyrotoxic patients the euthyroid PEP/LVET ratios were within the reference values. The systolic time intervals were not influenced by propranolol therapy in the thyrotoxic patients. Our results suggest increased myocardial contractility unaffected by adrenergic blockade in thyrotoxicosis, and reduced contractility in hypothyroidism.

Adult↗
PubMed1997

Systolic function, readmission rates, and survival among consecutively hospitalized patients with congestive heart failure.

We sought to describe the relation between left ventricular systolic function and rates of hospital readmission and survival among consecutively hospitalized patients with congestive heart failure. Medical records were reviewed for these patients at an academic medical center between Jan. 1, 1992, and Dec. 31, 1993. Left ventricular systolic function assessments performed within 6 months before discharge were used to classify left ventricular systolic function. Hospital readmission rates and survival through Dec. 31, 1994, were compared between patients with systolic dysfunction and those with preserved systolic function. Among 412 patients hospitalized with a primary diagnosis of congestive heart failure, 224 had undergone a left ventricular function assessment during the 6 months before hospital discharge. In-hospital mortality and readmission rates were higher among patients without a recent assessment of left ventricular systolic function. Of patients with systolic dysfunction, 55% versus 41% of patients with preserved systolic function were either readmitted or had an emergency room visit within 6 months after discharge (p = 0.06). At 27 months' follow-up, cumulative survival probabilities were 65% for patients with preserved systolic function, 65% for patients with systolic dysfunction, and 60% for patients without a left ventricular systolic function assessment (p = 0.24). Patients without a recent left ventricular systolic function assessment have significantly higher hospital readmission rates than patients with a recent systolic function assessment. Among hospitalized patients, mortality rates are comparable between patients with systolic dysfunction and those with preserved systolic function. However, patients with heart failure with systolic dysfunction may have higher readmission rates.

Aged↗
PubMed1998

Evaluation of the effect of haemodialysis on cardiac dysfunction in patients of chronic renal failure.

Thirty-eight patients with end stage renal disease who were on haemodialysis and had recurrent congestive cardiac failure were analysed. Echocardiographic findings were evaluated at start of haemodialysis and after 6 dialysis sessions. Seventeen cases (48%) had diastolic dysfunction, 11 (29%) systolic dysfunction 8 (18%) had normal echocardiogram and 2 (5%) had dilated left ventricle with normal ejection fraction. In the systolic dysfunction group the end diastolic diameter decreased after 6 dialysis sessions. In the diastolic dysfunction group the end diastolic diameter and ejection fraction decreased minimally. In the systolic dysfunction group 8 patients (42%) expired within 18 months with a mean survival of 5 months and in the diastolic dysfunction group 5 patients (28%) died within 18 months with a mean survival of 12 months.

Evaluation Studies as Topic↗
PubMed1990

Diastolic dysfunction of the left ventricle: importance to the clinician.

Diastolic dysfunction is a relatively common problem that may be mild and asymptomatic or may present with severe disabling symptoms. It is frequently due to coronary artery disease and/or LV hypertrophy and it is especially common in the older population. Patients with diastolic dysfunction and normal systolic function are best treated with calcium channel blocking agents or beta-blocking agents (drugs that are generally avoided in patients with significant systolic dysfunction). These drugs are used in the same dosage as is used in patients with angina or hypertension. Most treatment is based on symptomatic relief, and therefore periods of cautious trial and error are the rule. When diastolic dysfunction is associated with systolic dysfunction, it may be necessary to treat both conditions, but in general, positive inotropic agents and arterial vasodilators are not useful in patients with diastolic dysfunction.

Cardiomegaly↗