Left Ventricular Dysfunction in Diabetes

Patients with diabetes mellitus have a greater morbidity and mortality from cardiovascular disease than patients without diabetes. Concomitant hypertension and diabetes are associated with even greater risk of coronary disease, atherosclerotic and peripheral vascular disease, and congestive heart failure. In addition, an independent left ventricular dysfunction (diabetic cardiomyopathy) exists in patients with diabetes that may manifest itself initially as abnormalities in diastolic function but ultimately in systolic function. Firm evidence for this outcome exists experimentally, and reversal of systolic and diastolic abnormalities has been noted experimentally. The Diabetes Control and Complications Trial (DCCT) indicated that intensive glycemic control ameliorates microvascular complication of neuropathy, proteinuria, and retinopathy. Little evidence exists for macrovascular complications or for left ventricular dysfunction. Preliminary results of a canine study of glycemic control and left ventricular function are presented. Clinical correlates of this study and its results are meager. Determination of the role that glycemic control plays with regard to left ventricular systolic function and congestive heart failure awaits carefully controlled and designed clinical trials.     

Diabetic Cardiomyopathy in the Elderly

Diabetic cardiomyopathy is a microvascular disorder that occurs in diabetics that may lead to congestive heart failure (CHF) in the absence of hypertension, coronary artery disease, or valvular heart disease. In a large study of elderly subjects with 865 men and 1872 women, mean age 81?±?9 years, CHF developed in 272 of 690 diabetics (39 %) and in 467 of 2047 nondiabetics (23 %) (P?<?0.0001) at 43-month follow-up. Cox regression analysis showed that diabetes mellitus (risk ratio = 1.34, P?=?0.0003) was an independent significant predictor of time to development of CHF. For each 1 % increase in hemoglobin A1c, in 25,958 men and 22,900 women with diabetes, there was an 8 % increased risk of CHF (95 % CI, 5 %–12 %). The pathologic substrate of diabetic cardiomyopathy is characterized by myocardial damage, left ventricular hypertrophy, interstitial fibrosis, structural and functional changes of the coronary vessels, metabolic abnormalities, and autonomic cardiac neuropathy.     

卡维地洛治疗充血性心力衰竭的临床研究

目的观察卡维地洛对充血性心力衰竭(CHF)左心功能的影响。方法患冠心病、原发性高血压、扩张型心肌病的CHF患者共174例随机分为治疗组和对照组各87例,治疗组在强心、利尿、血管紧张素转换酶抑制剂(A-CEI)治疗的基础上,每天给卡维地洛6.25~50mg口服治疗,疗程24周。作治疗前、后NYHA分级、心功能的对照。结果治疗后NYHA分级、心功能均得到改善。结论卡维地洛治疗CHF 24周后,能抑制CHF的恶化,改善心功能,改善生活质量。     

Hyperthyroidism: a "curable" cause of congestive heart failure--three case reports and a review of the literature

With the increasing incidence of coronary artery disease and the aging population, the prevalence of congestive heart failure (CHF) is increasing. In the majority of these cases the etiology is underlying coronary artery disease. Other less common causes of CHF include valvular heart disease, hypertension, alcoholic cardiomyopathy, and dilated cardiomyopathy. In addition, there are rare causes, one of which is hyperthyroidism. Hyperthyroidism can affect the cardiovascular system in a variety of ways. The cardiovascular manifestations range from sinus tachycardia to atrial fibrillation and from a high cardiac output state to CHF due to systolic left ventricular dysfunction. If the underlying hyperthyroidism is recognized and treated early the CHF in such cases can be cured. The authors present three cases of CHF due to systolic left ventricular dysfunction secondary to hyperthyroidism, which showed considerable improvement in the left ventricular function once the hyperthyroidism was treated.     

Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.     

Diastolic dysfunction in exercise and its role for exercise capacity

Diastolic dysfunction is frequent in elderly subjects and in patients with left ventricular hypertrophy, vascular disease and diabetes mellitus. Patients with diastolic dysfunction demonstrate a reduced exercise capacity and might suffer from congestive heart failure (CHF). Presence of symptoms of CHF in the setting of a normal systolic function is referred to as heart failure with normal ejection fraction (HFNEF) or, if evidence of an impaired diastolic function is observed, as diastolic heart failure (DHF). Reduced exercise capacity in diastolic dysfunction results from a number of pathophysiological alterations such as slowed myocardial relaxation, reduced myocardial distensibility, elevated filling pressures, and reduced ventricular suction forces. These alterations limit the increase of ventricular diastolic filling and cardiac output during exercise and lead to pulmonary congestion. In healthy subjects, exercise training can enhance diastolic function and exercise capacity and prevent deterioration of diastolic function in the course of aging. In patients with diastolic dysfunction, exercise capacity can be enhanced by exercise training and pharmacological treatment, whereas improvement of diastolic function can only be observed in few patients.     

Diabetic cardiomyopathy: concept,heart function,and pathogenesis

The diabetic cardiomyopathy is a disease caused by diabetes and is characterised by the presence of diastolic and/or systolic left ventricular dysfunction. Diabetes may produce metabolic alterations, interstitial fibrosis, myocellular hypertrophy, microvascular disease and autonomic dysfunction. It is thought that all of them may cause cardiomyopathy. Other abnormalities that are usually associated with diabetes such as hypertension, coronary artery disease and nephropathy should be excluded before diagnosing diabetic cardiomyopathy. There is no evidence that diabetic cardiomyopathy alone can produce heart failure. However, subclinical ventricular dysfunction has been described in young asymptomatic diabetic patients without other diseases that could affect the cardiac muscle. In these cases we should consider that diabetes is the only cause of the myocardial disease. More studies are needed to know the natural history of diabetic cardiomyopathy.     

Diabetic cardiomyopathy

Diabetes mellitus is associated with a specific cardiomyopathy. This is evident from the clinical-pathological work and the epidemiologic data from the Framingham study. Noninvasive studies of diabetics have shown alterations in systolic and diastolic function that may ultimately lead to clinical heart failure. The relationship of these cardiac changes to the type of diabetes, its duration, and its severity is not settled. However, a correlation between changes in heart function and other complications of diabetes has been demonstrated. Insufficient prospective data is available from noninvasive studies to establish the frequency of progression from subclinical cardiac dysfunction to overt congestive failure. The pathogenesis of this disorder is still uncertain. Pathological studies have shown changes in the intramural arteries, arterioles, and capillaries but their functional significance is uncertain. Experimental studies have shown interstitial changes leading to an apparently less compliant left ventricle in the diabetic dog and monkey. In the diabetic rat reversible changes were found in myocardial function, related to changes in contractile proteins and intracellular calcium metabolism. In both species, the response to anoxia or ischemia was altered in the presence of diabetes. However, irreversible depression of the contractile element was not found in most animal studies of isolated diabetes. In contrast, the combination of hypertension and diabetes leads to substantial cardiac damage and circulatory congestion, both in clinical and experimental investigations. Clearly much more work must be carried out to understand the pathogenesis, treatment, and ultimately the prevention of diabetic cardiomyopathy.     

Arterial hypertension and systolic left ventricular dysfunction: therapeutic approach

Arterial hypertension is a cardinal precursor of congestive heart failure, and diastolic dysfunction is the most frequent mechanism for it. Systolic left ventricular dysfunction, although less frequent, has a worse prognosis. Most cases of systolic dysfunction in patients with hypertension is due to acute myocardial infarction, although other mechanisms can be involved. In some studies, non-ischemic hypertensive systolic dysfunction is the etiology of chronic heart failure in up to 10% of patients with dilated cardiomyopathy. Diastolic dysfunction and left ventricular hypertrophy are also associated with a higher risk of heart failure and systolic dysfunction. Given the poor prognosis of patients with congestive heart failure and dilated cardiomyopathy, it is fundamental to try to prevent the development of left ventricular dysfunction by means of a correct control of blood pressure, regression of left ventricular hypertrophy and prevention of coronary artery disease. When systolic dysfunction is established, angiotensin converting enzyme inhibitors are the treatment of choice; diuretics and digoxin can be added in patients with overt congestive heart failure. Recent studies suggest that other drugs, such as carvedilol and losartan, can be beneficial, but current evidence is still scarce.     

Cardiac resynchronization: a novel therapy for heart failure

Despite advances in medical therapy for patients with congestive heart failure, morbidity and mortality remain high. Conduction abnormalities, such as left bundle branch block, right bundle branch block, and nonspecific conduction delay, are observed commonly in patients with dilated cardiomyopathy. In patients with heart failure, the presence of intraventricular conduction delay is associated with more severe mitral regurgitation and worsened left ventricular systolic and diastolic function, and is an independent risk factor for increased mortality. Conventional dual-chamber (right atrial and right ventricular) pacing with a short atrioventricular delay was initially introduced as therapy for patients with advanced congestive heart failure to improve diastolic dysfunction and reduce mitral regurgitation. The acute beneficial hemodynamic effects observed in early, uncontrolled studies were not confirmed in subsequent randomized, controlled studies with longer follow-up. Cardiac resynchronization with novel biventricular (left and right ventricular) pacing systems has resulted in hemodynamic and functional benefits in patients with congestive heart failure and an underlying intraventricular conduction delay. Improvements in cardiac index, systolic blood pressure, and functional class have been reported with biventricular pacing, both acutely and at more than 1 year of follow-up. These encouraging preliminary results with biventricular pacing in patients with congestive heart failure will be validated in two prospective, randomized, controlled trials, Multicenter InSync Randomized Clinical Evaluation (MIRACLE) and Comparison of Medical Therapy, Pacing, and Defibrillation in Chronic Heart Failure (COMPANION). These studies are designed to evaluate the long-term efficacy of biventricular pacing in improving exercise capacity and in reducing morbidity and mortality in patients with advanced, symptomatic congestive heart failure. (c)2001 by CHF, Inc.     

Congestive heart failure in the elderly--echocardiographic insights.

One hundred and seventy-two patients (110 were greater than or equal to 65 years and 62 were less than 65 years) with congestive heart failure (CHF) were prospectively evaluated to determine various pathophysiologic mechanisms of CHF. The incidence of CHF with normal left ventricular (LV) systolic function was higher in elderly (30% vs 12%, p less than 0.05). Of the 110 elderly patients, LV systolic function was impaired in 77. Fifty-five patients had LV dilatation without increased wall thickness, and the clinical diagnosis was "dilated cardiomyopathy in the elderly". Twenty-two patients had hypertrophied LV and a high incidence of hypertension, and they were diagnosed as "hypertensive heart failure" due to contractile dysfunction. On the contrary, the remaining 33 patients did not have impaired LV contractile function. Thirteen patients lacking LV hypertrophy had enlarged atria. CHF was induced by reduced chamber compliance called "the stiff heart syndrome". Twenty patients had hypertrophied LV and a high incidence of hypertension. They were diagnosed as having "hypertensive hypertrophic cardiomyopathy of the elderly" and abnormalities of diastolic function accounted for the CHF. Since echocardiography can easily and accurately diagnose the pathophysiologic mechanism of CHF, an increased awareness of its occurrence in the elderly and use of echocardiography would reduce diagnostic and therapeutic errors.     

Prevalence of Suspected Diastolic Dysfunction in Patients with a Clinical Diagnosis of Congestive Heart Failure

Introduction: The prevalence of diastolic left ventricular (LV) dysfunction in a population presenting with a suspected diagnosis of congestive heart failure (CHF) is questionable and widely variable in the current literature. To minimize the disparity, we evaluated a large echocardiographic database to investigate the prevalence of systolic and suspected diastolic LV dysfunction in those with a suspected clinical diagnosis of CHF. Methods: We retrospectively reviewed echocardiograms performed at our institution and evaluated the prevalence of abnormal LV systolic and diastolic function in those with a suspected clinical diagnosis of CHF. Diastolic dysfunction was defined as the presence of left atrial enlargement, left ventricular hypertrophy and reverse trans-mitral inflow ratio (E/A reversal). Results: Of the 636 echocardiograms with CHF as the primary diagnosis, 461 had measured LV function. Normal LV systolic function were found in 238 of the patients (48%). Isolated diastolic LV dysfunction was found in 166 patients (36%). Twelve percent of the patients with a suspected clinical diagnosis of CHF had normal LV systolic and diastolic function. Conclusion: Normal LV systolic function was seen in nearly one-half of the echocardiograms with a suspected clinical diagnosis of CHF. Suspected LV diastolic dysfunction was observed in one-third of the echocardiograms with a suspected clinical diagnosis of CHF.     

Management of obesity cardiomyopathy

Therapy of acute exacerbations of congestive heart failure associated with obesity cardiomyopathy consists of dietary salt restriction, inspired oxygen, diuretics, and angiotensin-converting enzyme inhibitors or, if left ventricular systolic dysfunction is present, hydralazine/isosorbide dinitrate. Digitalis may be indicated in selected cases. These measures may also be useful chronically in association with weight loss. Substantial weight loss is capable of reversing all of the hemodynamic abnormalities associated with obesity except elevation of left ventricular filling pressure. Substantial weight loss may also reduce left ventricular mass and improve left ventricular diastolic filling in those with left ventricular hypertrophy before weight loss. Left ventricular systolic function also improves after weight loss in those with impaired pre-weight-loss systolic function. These beneficial effects of weight loss occur partly because of favorable alterations in left ventricular loading conditions. Substantial weight loss in patients with congestive heart failure associated with obesity cardiomyopathy produces a reversal of many of the clinical manifestations of cardiac decompensation and improves New York Heart Association functional class in most patients.     

Pregnancy-induced severe left ventricular systolic dysfunction in a patient with hypertrophic cardiomyopathy

This paper reports the first case of hypertrophic cardiomyopathy (HCM) that developed postpartum congestive heart failure (CHF) and severe left ventricular (LV) systolic dysfunction. Review of the literature and clinical implications are discussed.     

Comparison of left ventricular function by tissue Doppler imaging in patients with diabetes mellitus without systemic hypertension versus diabetes mellitus with systemic hypertension

Because diabetes mellitus substantially increases the risk of development of heart failure, we sought to establish early alterations in left ventricular systolic and diastolic function in patients with diabetes mellitus with and without coexisting systemic hypertension. We studied 134 subjects using echocardiography comprising standard 2-dimensional and conventional Doppler as well as tissue Doppler imaging. Our study demonstrated the early appearance of both left ventricular systolic and diastolic dysfunction in diabetic patients at rest and the contributory effects of diabetes to myocardial impairment produced by hypertension, as well as the high usefulness of tissue Doppler imaging in detection and quantitation of myocardial dysfunction in diabetics. This method was superior to other echocardiographic techniques and plasma brain natriuretic peptide evaluation.     

Clinical assessment and follow-up of functional capacity in patients with chronic congestive cardiomyopathy

The presumption that the results of left ventricular systolic function tests performed at rest are related to the symptoms of chronic congestive heart failure or to exercise capacity is unproved. Thirty-three patients with chronic congestive Cardiomyopathy underwent serial exercise tests, determinations of ejection fraction and systolic time intervals, echocardiograms, assessment of symptom score, chest roentgenogram, and physical examination over a mean (± standard deviation) of 24.8 ± 14.1 months. Maximal exercise performance achieved correlation with symptoms (r = −0.66) but not with indexes of left ventricular function. Edema, elevated jugular venous pressure, rales and radiologic evidence of pulmonary venous hypertension were more common in patients with severe limitation of exercise capacity. In 17 patients whose functional capacity changed during the follow-up period, congruent changes in left ventricular function measured at rest were not consistently observed.

Thus the findings on history, physical examination and radiologic examination correlate with exercise capacity, but indexes of left ventricular performance at rest do not and therefore are of limited use in assessing treatment. The clinical course of patients with chronic congestive cardiomyopathy can be followed up safely, effectively and economically by simple clinical observations. Serial laboratory testing of left ventricular function can be reserved for specific indications, research and patients with valvular heart disease.     

Systolic and diastolic heart failure--diagnostic and therapeutic dilemmas

Clinical suspicion of congestive heart failure (CHF) always requires a careful diagnostic workup. This comprises the verification of the presence of CHF (in contrast to other conditions that cause nonspecific phenomena such as shortness of breath and edema), evaluation of the underlying cause of heart failure, and assessment of left ventricular (LV) systolic function. In addition to clinical examination, echocardiography is warranted in most cases. On the basis of this information, patients can be selected for further studies, such as exercise testing, cardiac catheterization and coronary angiography. In view of the serious prognosis of heart failure, especially systolic CHF, the threshold for specialist consultation should be low. Although the classification of CHF into systolic and diastolic forms is complex, clinically meaningful data can be derived simply by determining whether LV systolic function is impaired (predominantly systolic CHF) or not (probable diastolic CHF). In the latter case, treatment is mainly symptomatic in addition to the management of the underlying condition (e.g. hypertension). In systolic CHF, considerable therapeutic advances have recently been made and it is important that patients receive appropriate care to improve their prognosis. These measures include angiotensin-converting enzyme inhibitors, beta-blockers and spironolactone.     

Plasma norepinephrine in congestive heart failure.

Resting plasma concentrations of norepinephrine, dopamine-beta-hydroxylase enzyme activity and peripheral blood lymphocyte beta adrenergic receptor sensitivity to isoproterenol as reflected in cyclic 3′,5′-adenosine monophosphate (cAMP) generation were studied in patients with congestive heart failure due to atherosclerotic heart disease or to congestive cardiomyopathy or hypertensive cardiovascular disease. Systolic time Intervals were also measured in nonhypertensive patients and correlated with the plasma norepinephrine concentration. Control patients were hospital employees without a previous history of heart disease or hypertension, and were matched for age to eliminate the effect of increasing age on the plasma norepinephrine concentration.The results of this study clearly demonstrate that the plasma norepinephrine concentration is directly related to the degree of left ventricular dysfunction in patients with congestive heart failure. When the systolic time intervals were correlated with the plasma norepinephrine levels, a significant prolongation of the preejection period was observed with progressively increasing plasma concentrations of norepinephrine. The reverse was true for the left ventricular ejection time, which demonstrated a significant Inverse relation with the plasma norepinephrine concentration. The ratio of the preejection period to the left ventricular ejection time, which is a reflection of left ventricular function, significantly increased with increasing levels of plasma norepinephrine. In addition, plasma lymphocytes from patients with the greatest degree of left ventricular dysfunction failed to generate normal amounts of cAMP after beta adrenergic receptor stimulation with isoproterenol. It Is suggested that beta adrenergic receptors are desensitized in these patients and that this desensitization contributes to the observed alterations in myocardial contractility.     

Left ventricular function in diabetes mellitus. I: Methodology, and prevalence and spectrum of abnormalities.

Frequent abnormalities of left ventricular function were detected in 212 established diabetic patients using non-invasive techniques. Diabetics without angina or heart failure (n = 185) were significantly different from normal subjects (n = 50) in beat-to-beat variation, ratio of pre-ejection period to left ventricular ejection time, pre-ejection period index, isovolumic relaxation time, and interval from minimal dimension to mitral valve opening. Diabetics with angina (n = 18) were similar to control subjects with angina (n = 25); they showed a significant dimension change during the isovolumic period as compared with other diabetics and normals. Sixteen diabetics without angina also showed outward motion during the isovolumic period (incoordinate relaxation) and 13 had abnormal systolic time intervals. Four diabetics suffered a myocardial infarction during the study period; all had previously shown incoordination. Comparison of diabetics with a diastolic blood pressure below 100 mmHg and between 100 and 125 mmHg showed that the latter had a thicker posterior wall; the enlarged systolic dimension and reduced fractional shortening were the result of the inclusion of five of the 11 diabetic subjects with heart failure in the hypertensive group. Insulin-dependent diabetics tend to have more pronounced abnormalities of left ventricular function than those not requiring insulin. Patients selected from a diabetic clinic frequently have impaired left ventricular function, and ventricular hypertrophy, when present, in primarily caused by hypertension.     

The Prevalence of Diabetic Cardiomyopathy: A Population-Based Study in Olmsted County,Minnesota

BackgroundDiabetic cardiomyopathy defined as either systolic or diastolic dysfunction in otherwise healthy diabetic persons is not clearly understood. The prevalence and outcomes of this disease in a community-based population have not been defined.Methods and ResultsCross-sectional survey of 2042 randomly selected residents of Olmsted County, Minnesota, aged 45 years or older between June 1997 and September 2000. All patients underwent Doppler echocardiographic assessment of systolic and diastolic function. Diabetic cardiomyopathy was defined in a person with diabetes and any systolic or at least moderate diastolic dysfunction without a history of coronary disease, hypertension, significant valvular disease, or congenital heart disease. The diagnosis of diabetic cardiomyopathy was made in 23 people, corresponding to a community population prevalence rate of 1.1%. Among diabetic patients, 16.9% met criteria for diabetic cardiomyopathy and 54.4% had diastolic dysfunction. Diabetes was associated with a 1.9-fold increase in risk of any left ventricular dysfunction, a 1.7-fold increase in risk of diastolic dysfunction, and a 2.2-fold increase in risk of systolic dysfunction. Among patients with diabetic cardiomyopathy, the cumulative probability of death was 18%, development of heart failure was 22%, and development of death or heart failure was 31% at 9 years.ConclusionDiabetic cardiomyopathy is relatively common in the community with a prevalence of 1.1%. The morbidity and mortality of patients with diabetic cardiomyopathy is high.