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PubMed1989

[Aortic stenosis with left ventricular systolic dysfunction: a severe disease but with good surgical prognosis].

From our series of 72 patients with severe valvular aortic stenosis, we identified 19 showing features of left ventricular systolic disfunction (ventriculographic ejection fraction less than 55% and/or fractional shortening less than 30% at M-mode echocardiography). In these patients, we found a significant inverse correlation between the fractional shortening and the systolic wall stress (r = 0.79, p less than 0.001). Clinically, 18 of the 19 patients were in NYHA class III (n = 11) or IV (n = 5), and two died before they could be operated upon. The remaining 17 had their aortic valve replaced (coronary artery bypass surgery was simultaneously performed in 2 patients). After a mean follow-up of 18 months, all patients are alive and show substantial symptomatic improvement (15 patients in class I and 2 patients in class II). Cardiothoracic index was reduced (61 +/- 5% preoperatively versus 52 +/- 5% postoperatively), and fractional shortening changed from 21 +/- 5% to 30 +/- 5%. The latter remains under normal limits in two thirds of the patients. Our results lend support to the idea that the systolic left ventricular dysfunction in aortic stenosis is due to the increased afterload, rather than to an intrinsic contractility defect. This explains the great functional improvement after the reduction of the systolic wall stress achieved by surgery.

Adult↗
PubMed1982

The role of right ventricular systolic dysfunction and elevated intrapericardial pressure in the genesis of low output in experimental right ventricular infarction.

To elucidate the pathophysiology of severe right ventricular infarction (RVI), isolated RVI was produced in 15 dogs with the pericardium intact or open. After RVI in dogs with the pericardium intact, RV systolic pressure decreased by 27%, aortic pressure by 29% and cardiac output by 34%. RV transmural pressure, RV end-diastolic size and intrapericardial pressure increased, left ventricular transmural pressure and end-diastolic size decreased and the diastolic pressures equalized. Pericardiotomy after RVI resulted in increased ventricular transmural pressures and diastolic size, improved cardiac output and resolution of equalized diastolic pressures. RVI in dogs with the pericardium open resulted in similar changes, but of lesser magnitude and without equalization of diastolic pressures. These results indicate that reduced left ventricular preload due to impaired RV systolic function contributes to low cardiac output in RVI. Elevated intra-pericardial pressure further reduced left ventricular preload and produces equal diastolic pressures.

Animals↗
PubMed1995

Residual exertional ischemia and unfavorable left ventricular remodeling in patients with systolic dysfunction after anterior myocardial infarction.

OBJECTIVES: This study investigated whether exercise-induced myocardial ischemia influences left ventricular remodeling after anterior myocardial infarction. BACKGROUND: The effects of acute and recurrent ischemia on ventricular function are well established. However, to our knowledge the role of exertional ischemia in the remodeling response after infarction has not been investigated. METHODS: Ninety-one patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy. The echocardiographic examination was repeated 6 months later. On the basis of the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were assigned to groups with no exertional ischemia (group 1, n = 20 [22%], mild to moderate ischemia (group 2, n = 45 [49%]) and severe exertional ischemia (group 3, n = 26 [29%]). RESULTS: Initial left ventricular volumes were similar, and no differences were found among the three groups in the remodeling response over the 6-month period of the study. However, patients in groups 2 and 3 with an ejection fraction < or = 40% showed significant (p < 0.01) ventricular enlargement over time, which was similar between the two groups (end-diastolic volume [mean +/- SD] from 74 +/- 13 to 80 +/- 17 ml/m2 in group 2 and from 72 +/- 11 to 81 +/- 19 ml/m2 in group 3; regional dilation from 42 +/- 16% to 52 +/- 22% in group 2 and from 38 +/- 18% to 46 +/- 27% in group 3). In contrast, ventricular dimensions did not change in group 1 patients with an ejection fraction < or = 40% as well as in patients in all three groups with an ejection fraction > 40%. CONCLUSIONS: Exercise-induced myocardial ischemia may contribute to progressive ventricular enlargement in patients with poor left ventricular function after a large anterior myocardial infarction.

Analysis of Variance↗
PubMed1992

[A case of hypereosinophilic syndrome exhibiting left ventricular systolic dysfunction].

A 16-year-old woman suffering from bronchial asthma since 2 years previously was admitted to the hospital because of high grade fever, dyspnea, skin eruption and arthralgia. Laboratory data revealed pronounced eosinophilia with elevated immunoglobulin E value. A chest X-ray film showed cardiomegaly with pulmonary congestion. Left ventriculograms showed diffusely reduced motion of the left ventricle (LV). Various clinical symptoms and laboratory data were resolved shortly after the administration of corticosteroids, but the LV dysfunction persisted for at least three months. Left ventriculograms 2 years later disclosed a marked improvement of the LV wall motion. In both the acute and the chronic phase, endomyocardial biopsy of both ventricles revealed non-specific histological findings comprising disarrangement of myocytes and interstitial fibrosis, suggesting post-myocarditis. This case was characterized by LV dysfunction possibly due to eosinophilic myocarditis associated with hypereosinophilic syndrome, and by its functional improvement with long-term corticosteroid therapy.

Adolescent↗
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↗
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

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↗