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PubMed1990

Influence of glucose and insulin on the exaggerated diastolic and systolic dysfunction of hypertrophied rat hearts during hypoxia.

Myocardial hypertrophy can result in increased sensitivity toward the development of mechanical dysfunction during hypoxia. Alterations in glycolytic metabolism may contribute to this. We studied the response to 15 minutes of hypoxia in hypertrophied (deoxycorticosterone-salt hypertension model) and nonhypertrophied rat hearts and examined the influence of a high glucose (27.5 mM) and insulin (100 mU/ml) concentration. In response to hypoxia in the presence of a normal glucose concentration (5.5 mM), left ventricular end-diastolic pressure was higher in hypertrophied than in nonhypertrophied hearts (65 +/- 6 vs. 44 +/- 4 mm Hg; p less than 0.05). Perfusion with high glucose and insulin blunted the rise in left ventricular end-diastolic pressure in both hypertrophied and nonhypertrophied hearts and abolished the difference in diastolic dysfunction between groups during hypoxia (26 +/- 2 vs. 32 +/- 4 mm Hg, respectively; p = NS). At end hypoxia in the presence of a normal glucose concentration, developed pressure was more depressed in hypertrophied than in nonhypertrophied hearts (11 +/- 1 vs. 18 +/- 1% of baseline, respectively; p less than 0.05). Perfusion with high glucose and insulin resulted in improved function in both groups during hypoxia such that a greater impairment of developed pressure was no longer present in the hypertrophied versus nonhypertrophied hearts (21 +/- 1 vs. 24 +/- 2% of baseline, respectively; p = NS). At the end of hypoxic perfusion in the presence of a normal glucose concentration, hypertrophied hearts were producing 38% less lactate than nonhypertrophied hearts. Perfusion with high glucose and insulin increased lactate production in both groups and equalized lactate production between groups. Thus, the greater deterioration in hemodynamic function in hypertrophied hearts compared with nonhypertrophied hearts during hypoxia is associated with lower lactate production. Both the exaggerated hemodynamic dysfunction and deficient lactate production can be ameliorated by perfusion with a high glucose concentration and insulin.

Animals↗
PubMed1990

Thallium 201 kinetics in stunned myocardium characterized by severe postischemic systolic dysfunction.

The hypothesis tested in this study was that despite the presence of severe postischemic myocardial dysfunction ("stunning"), the extraction and subsequent intracellular washout of thallium 201 should be preserved as long as irreversible sarcolemmal membrane injury was avoided. To produce myocardial stunning, 19 open-chested dogs with a critical left anterior descending coronary artery (LAD) stenosis underwent 10 5-minute periods of total LAD occlusion, each interspersed by 10 minutes of reperfusion by reflow through the critical stenosis. In another 12 control dogs observed for the same time period, no LAD occlusions were performed after placement of the critical stenosis. Hemodynamics, regional myocardial thickening by quantitative two-dimensional echocardiography, and microsphere-determined regional blood flows were serially measured. In 18 stunned dogs, systolic thickening in the LAD zone was markedly reduced to 0.4 +/- 2.4% at 40 minutes after the 10th reperfusion period compared with 32.5 +/- 2.2% thickening (p less than 0.001) in 12 control dogs at a matched time. The 201Tl first-pass extraction fraction determined by a double-isotope method using intracoronary 201Tl administration was comparable after the 10th reflow in a subgroup of 13 stunned (0.78) and six control (0.79) dogs. The T1/2 for the intracellular washout rate was also not significantly different in another group of six stunned (60 +/- 13 minutes) and six control (53 +/- 14 minutes) dogs, nor was the percentage of the 201Tl dose initially distributed in the interstitial compartment (11 +/- 3% vs. 7 +/- 2%). Systemic hemodynamics and regional flows were comparable in the two groups at 40 minutes after the 10th reflow. No dog had evidence of myocardial necrosis by triphenyl tetrazolium chloride staining. Thus, normal myocardial 201Tl extraction and washout kinetics are observed in a canine model of severe postischemic dysfunction (stunning) produced by repetitive brief LAD occlusions. These findings might have important clinical implications concerning the application of rest 201Tl scintigraphy for evaluation of perfusion and viability in patients with coronary artery disease and regional myocardial asynergy that is ultimately reversible.

Animals↗
PubMed1993

Is left ventricular systolic dysfunction in hypertensive patients with heart failure normalized by long-term antihypertensive therapy?

The critical left ventricular (LV) mass when hypertensive heart failure appears, and whether LV dysfunction in hypertensives with heart failure is normalized by long-term antihypertensive therapy were investigated. LV dimension, LV mass, LV mass index, LV ejection time (LVET) and pre-ejection period (PEP) were measured in 27 normal subjects and 56 essential hypertensives, the latter divided into three groups: group I, without LV hypertrophy; group II, with LV hypertrophy; and group III, with hypertensive heart failure. LV mass and LV mass index were 135.0 +/- 23.8 g and 85.8 +/- 11.7 g/m2, respectively, in normal controls, 133.0 +/- 30.8 g and 82.0 +/- 18.4 g/m2 in group I, 222.3 +/- 38.0 g and 136.1 +/- 19.9 g/m2 in group II, and 422.0 +/- 30.3 g and 235.7 +/- 19.6 g/m2 in group III of essential hypertensives. The upper limits of LV mass and LV mass index in group II (mean + 2SD) were about 300 g and 180 g/m2, respectively. Significant shortening of LVET was observed only in group III, but PEP was prolonged with an increase in LV mass. LV diastolic dimension and PEP were not normalized by long-term antihypertensive therapy (mean: 16 months). These results indicate that the critical LV mass marking the transition from non-failing hypertrophied left ventricle to failing ventricle associated with essential hypertension is about 300 g, or LV mass index of 180 g/m2, and that LV dilatation and depressed myocardial contractility in essential hypertensives with a past history of congestive heart failure were not normalized by chronic antihypertensive therapy.

Adult↗
PubMedDate not supplied

Management of heart failure. IV. Anticoagulation for patients with heart failure due to left ventricular systolic dysfunction.

OBJECTIVE: This article reviews the incidence of arterial thromboembolism in patients with heart failure who are not receiving anticoagulants. We also examine whether more severe ventricular dysfunction increases this incidence and the efficacy and risks of anticoagulation for patients in sinus rhythm. DATA SOURCES: English-language studies referenced in MEDLINE or EMBASE (January 1966 to September 1993) were reviewed. We used the search terms heart failure, congestive; congestive heart failure; heart failure; cardiac failure; and dilated cardiomyopathy in conjunction with the terms anticoagulation, cerebrovascular disorders, stroke, and thromboembolism. STUDY SELECTION: All studies with separate data for patients with chronic heart failure not receiving anticoagulants were included. Articles addressing valvular heart disease or heart failure secondary to acute myocardial infarction or Chagas' disease were excluded. Studies of the occurrence of left ventricular mural thrombi were also reviewed. DATA EXTRACTION AND SYNTHESIS: Inclusion and exclusion criteria, prevalence of atrial fibrillation, mean follow-up, and the occurrence of arterial thromboembolic events were extracted. If the incidence was not given, this was estimated using the proportion of patients with events divided by the mean follow-up. CONCLUSION: The incidence of arterial thromboembolism ranged from 0.9 to 5.5 events per 100 patient-years, with the largest studies reporting incidence of 2.0% and 2.4%. Findings regarding the relationship between ventricular function and thromboembolic events are contradictory. No controlled trial has assessed the efficacy or risks of anticoagulation for patients with heart failure and sinus rhythm, and reported efficacy in case series ranged from 0% to 100%. Until adequate studies are performed, anticoagulation should be discouraged for patients with heart failure who are in sinus rhythm.

Anticoagulants↗
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↗
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↗
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↗
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↗
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↗
PubMed1995

Hospitalized congestive heart failure patients with preserved versus abnormal left ventricular systolic function: clinical characteristics and drug therapy.

PURPOSE: To compare clinical characteristics of and pharmacologic therapy for hospitalized patients with congestive heart failure (CHF) and left ventricular systolic dysfunction or normal left ventricular systolic function. PATIENTS AND METHODS: Medical records were reviewed for all patients discharged with a principal diagnosis of CHF from a university hospital and a community hospital between September 1, 1991 and August 31, 1992. Pertinent medical history items and prescribed drug therapies at discharge were recorded for each patient's first calendar year admission. Patients were categorized as having either normal left ventricular systolic function or systolic dysfunction based on the results of echocardiography and radionuclide angiography or contrast ventriculogram. RESULTS: Of 298 patients with CHF, 92 (31%) had normal left ventricular systolic function. Patients with normal systolic function were older, were more often women, were less likely to have a history of coronary artery disease, and were more likely to have a history of hypothyroidism than patients with systolic dysfunction. However, the prevalence of clinical characteristics overlapped considerably between the two groups. Among patients with systolic dysfunction, 79% were discharged on a therapeutic regimen of digoxin, 65% on an angiotensin-converting enzyme inhibitor, and 26% on either a beta-blocker or a calcium channel blocker. Among patients with normal systolic function, 50% were discharged on a regimen of a beta-blocker or a calcium channel blocker and 38% were discharged on digoxin. Twenty-six percent of patients with normal systolic function and without a history of atrial fibrillation were discharged on a digoxin regimen. CONCLUSION: Hospitalized CHF patients with normal left ventricular systolic function and those with diminished left ventricular systolic function share many clinical features. Since recommended drug therapy and prognosis differ, our data underscore the importance of diagnostic testing to assess left ventricular systolic function. Drug therapy for CHF patients provides a major challenge for quality-of-care improvement.

Aged↗
PubMed1991

Prevalence of unsuspected mitral regurgitation and left ventricular diastolic dysfunction in patients with coronary artery disease and acute pulmonary edema associated with normal or depressed left ventricular systolic function.

To define the prevalence and role of left ventricular (LV) systolic dysfunction, LV diastolic dysfunction and mitral regurgitation (MR) in patients with acute pulmonary edema, 40 patients with coronary artery disease and acute pulmonary edema were prospectively evaluated within 36 hours of presentation. LV ejection fraction and 3 parameters of LV diastolic function were measured with radionuclide ventriculography, whereas MR was assessed with Doppler echocardiography. LV ejection fraction was normal in 11 (27%) and depressed in 29 (73%) patients. Moderate or severe MR without LV diastolic dysfunction was common and equally prevalent in patients with and without LV systolic dysfunction (33 vs 38%; difference not significant). Diastolic dysfunction without MR was less frequent but equally prevalent in patients with and without systolic dysfunction (17 vs 27%; difference not significant). Two (18%) of 11 patients without and 12 (33%) of 36 patients with LV systolic dysfunction had both MR and LV diastolic dysfunction. Furthermore, MR was clinically silent and unsuspected in two-thirds of all patients with MR, regardless of a normal or depressed systolic function. These data show that there is a high prevalence of unrecognized moderate to severe MR in patients with acute pulmonary edema, regardless of the presence or absence of LV systolic dysfunction. Furthermore, the prevalence of LV diastolic dysfunction without MR is relatively low even in patients with normal LV systolic function and pulmonary edema. Thus, unrecognized MR may be an important contributor to the syndrome of acute pulmonary edema in patients with normal or depressed LV systolic function.

Aged↗
PubMed1993

Congestive heart failure: systolic and diastolic function.

There is increasing recognition that disorders of both left ventricular systolic and diastolic function can result in congestive heart failure. As such, consideration of both the filling and emptying characteristics of the left heart is needed to evaluate the hemodynamic abnormalities present in this syndrome. Considerations of the systolic (emptying) and diastolic (filling) pumping characteristics of the left heart also provides a conceptual basis to classify and understand the pathophysiology of congestive heart failure. In this context, systolic dysfunction can be defined as impaired emptying of the LV, apparent as a decreased (< 50%) effective ejection fraction (forward stroke volume divided by end-diastolic volume). Systolic dysfunction may result from impaired myocardial contractile function, increased left ventricular afterload, and/or structural abnormalities of the left heart. Diastolic dysfunction can be defined as a condition in which filling of the LV sufficient to produce an adequate cardiac output requires an elevated pulmonary venous pressure. Thus, diastolic dysfunction is clinically manifested as pulmonary congestion. Defined in this manner, the most common cause of diastolic dysfunction is systolic dysfunction. In fact, the most common symptom of patients with systolic dysfunction is dyspnea from the resulting diastolic dysfunction. Diastolic dysfunction in the setting of normal systolic function may be due to obstruction of left ventricular filling, impaired left ventricular distensibility, or extensive external compression of the LV. Treatment of diastolic dysfunction can be accomplished by relieving myocardial ischemia, improving systolic function, lowering arterial systolic pressure, and decreasing cardiac distention.

Cardiac Output↗