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PubMed1986

Persistence of regional left ventricular dysfunction after exercise-induced myocardial ischemia.

To determine whether regional myocardial dysfunction occurring after exercise-induced ischemic might be caused by continued abnormalities of myocardial blood flow in the post-exercise period, nine dogs were instrumented with ultrasonic microcrystals for determination of circumferential segment shortening, circumflex artery electromagnetic flow probes, and hydraulic coronary artery occluders. Dogs performed treadmill exercise during partial inflation of the coronary artery occluder. When the stenosis was maintained after exercise (persistent stenosis), subendocardial flow = 0.79 +/- 0.42 ml/min per g vs. 1.39 +/- 0.43 ml/min per g control), and this was associated with continued dysfunction in the ischemic zone (segment shortening 45.4 +/- 36.9% of resting control). When the stenosis was released immediately after exercise (temporary stenosis), however, flow was markedly increased 1 min post-exercise (mean transmural flow 4.24 +/- 1.22 ml/min per g; subendocardial flow 4.18 +/- 1.52 ml/min per g), and this was associated with a transient increase in segment shortening to 104.5 +/- 9.3% of resting control. 5 min after exercise, however, moderate reductions in ischemic segment shortening were noted after both temporary stenosis and persistent stenosis runs, and these persisted for 30 min post-exercise. It is concluded that regional left ventricular dysfunction may persist for a significant period of time after exercise-induced ischemia. Furthermore, early after exercise, dysfunction is related to persistent abnormalities of myocardial blood flow, whereas late after exercise it is independent of primary reductions in myocardial blood flow.

Animals↗
PubMedDate not supplied

Sestamibi SPECT in the detection of myocardial viability in patients with chronic ischemic left ventricular dysfunction: comparison between visual and quantitative analysis.

BACKGROUND: Technetium 99m sestamibi cardiac scintigraphy is widely used as a means of predicting myocardial viability in patients with chronic ischemic left ventricular (LV) dysfunction. No data are available comparing the results of visual and quantitative analysis of tomographic imaging in the assessment of myocardial viability. The aim of this study was to directly compare visual and quantitative analysis of resting sestamibi single photon emission computed tomography in the identification of viable myocardium in patients with chronic LV dysfunction. METHODS AND RESULTS: Sixty-five patients with an earlier myocardial infarction and LV dysfunction that had occurred within 1 week underwent echocardiography and resting sestamibi SPECT. In each patient, regional tracer distribution was visually assessed and quantitatively measured in 13 segments. Regional LV function was evaluated in corresponding segments by means of echocardiography. All patients underwent revascularization, and echocardiography was repeated 12 months later as a means of assessing the recovery of regional LV function. Among all akinetic or dyskinetic revascularized segments, 66 of 112 viable segments (59%) and 85 of 100 nonviable segments (81%) were identified by means of visual analysis. Eighty-two of 112 viable segments (73%; P<.05 vs. visual analysis) and 74 of 100 nonviable segments (74%; P = .3 vs. visual analysis) were identified by means of quantitative analysis, with a threshold of 55%. Receiver operating characteristic curve areas constructed by using visual and quantitative analyses for the detection of myocardial viability in all 212 akinetic or dyskinetic segments were 0.79+/-0.04 and 0.81+/-0.03, respectively (P = not significant). Overall concordance in the detection of myocardial viability between visual and quantitative analysis was observed in 165 of akinetic or dyskinetic dysfunctional segments (78%), with a kappa value of 0.6. CONCLUSIONS: The results of this study demonstrate that, in patients with chronic myocardial infarction and LV dysfunction, visual and quantitative analysis of sestamibi tomographic images at rest have similar overall accuracy in predicting the recovery of LV function after coronary revascularization procedures.

Chronic Disease↗
PubMed1978

The "false negative" treadmill exercise test and left ventricular dysfunction.

One hundred and fifteen consecutive symptomatic patients undergoing graded exercise testing, selective coronary angiography and left ventriculography were retrospectively evaluated. The sensitivity, specificity, and false negative response rates of the exercise tests were 79%, 81%, and 21%, respectively. Although the magnitude of a positive ST-segment response was related to more extensive vascular disease, the frequency of false negative responses was nearly identical in patients with single, double, or triple vessel disease (22%, 21%, 19%). Analysis of the false negative group demonstrated significant ventriculographic and hemodynamic abnormalities when compared to the true positive responders. Five out of six patients with the most serious motion disorders in the study fell into the false negative group. There were no significant differences in the extent, distribution and severity of vascular involvement, or in the development of collateral circulation in the two groups. However, occluded vessels supplied abnormal ventricular segments more frequently in the false negative group (88% vs 38%); the absence of an "ischemic response" and the presence of segments of abnormal myocardium may be related. Left ventricular dysfunction appears to be an important reason for a false negative response to exercise.

Angiography↗
PubMed2000

Subclinical left ventricular dysfunction in systemic hypertension and the role of 24-hour blood pressure.

The relation between blood pressure (BP) and left ventricular (LV) systolic function in systemic hypertension is controversial. We assessed the relation of LV midwall fractional shortening (FS) to 24-hour BP in 1,702 never-treated hypertensive subjects (age 48 +/- 12 years), who underwent 24-hour BP monitoring and echocardiography. Stress-corrected endocardial and midwall FS (the latter calculated taking into account the epicardial migration of midwall during systole) were predicted in hypertensives on the basis of the values observed in 130 healthy normotensives (age 43 +/- 13 years, office BP 126/78 mm Hg). Subjects below the fifth percentile of observed-to-predicted FS had depressed LV function. The use of midwall FS resulted in an increase from 3.5% to 17.5% in the proportion of patients with depressed chamber function. Compared with the group with normal function, subjects with low midwall LV function had similar office systolic BP (155 +/- 21 vs 154 +/- 17 mm Hg), but increased 24-hour systolic BP (140 +/- 17 vs 133 +/- 12 mm Hg, p <0.001). Midwall FS had a closer negative relation to 24-hour systolic BP than to office systolic BP (r = -0.27 vs -0.08, p <0.001), whereas this difference was not apparent for diastolic BP (r = -0.23 vs -0.20). Compared with endocardial FS, midwall FS had a stronger inverse association to LV mass (r = -0.45 vs -0.16, p <0.001). Thus, an increased 24-hour BP load may chronically lead to depressed myocardial function in systemic hypertension in the absence of clinically overt heart disease.

Adult↗
PubMed1998

A prolonged QRS duration on surface electrocardiogram is a specific indicator of left ventricular dysfunction [see comment].

OBJECTIVE: We sought to determine whether a prolonged QRS-interval duration is associated with decreased left ventricular (LV) systolic function. BACKGROUND: The 12-lead electrocardiogram (ECG) is a routine test for suspected cardiac disease. Although several scoring systems have been devised to estimate LV systolic function, no studies have examined the direct relationship between QRS duration alone and LV systolic function. METHODS: We analyzed the standard 12-lead surface ECG of 270 consecutive patients, referred for radionuclide ventriculography. Patients (n = 44) with bundle branch blocks, atrial flutter or fibrillation, pacemaker rhythm, recent myocardial infarction or bypass surgery, and patients on antiarrhythmic drugs were excluded. In the remaining patients (n = 226), we correlated the QRS duration on standard resting ECG, and the resting LV ejection fraction (EF), end-systolic and end-diastolic counts (ESC and EDC, respectively; LV volume indices), as obtained by radionuclide angiography. We used a multivariate analysis to identify independent predictors of reduced ventricular function entering QRS duration, the previously described R-wave score and clinical variables in our model. RESULTS: The QRS duration in the abnormal EF group was significantly longer than in the normal EF group (0.102 vs. 0.091 s, p < 0.0001). A QRS duration >0.10 s was highly specific (83.6%), but modestly sensitive (43.8%), for the prediction of abnormal EF. Furthermore, an abnormal EF was predicted with incrementally increased specificity (83.6% to 99.3%) and a corresponding decrease in sensitivity (43.8% to 13.8%) for each 0.01-s increase in the definition of prolonged QRS (from >0.10 to >0.12 s). Accordingly, the positive likelihood ratio for the prediction of decreased LV function was increased from 2.67 to 19.7 as the definition of prolonged QRS duration was increased from >0.10 to >0.12 s. In the multivariate analysis, a prolonged QRS duration and a low R-wave score were the only independent predictors of decreased LV systolic function. CONCLUSIONS: Prolonged QRS duration (>0.10 s) obtained from a standard resting 12-lead ECG is a specific, but relatively insensitive indicator of decreased LV systolic function. Further prolongation of the QRS had a higher specificity for decreased LV EF and a higher positive likelihood ratio for predicting abnormal LV EF.

Arrhythmias, Cardiac↗
PubMed1985

The analysis of systolic and diastolic time intervals: a more sensitive non-invasive method in the assessment of left ventricular dysfunction in the patients with essential hypertension.

Time indices and volumetric parameters were investigated in patients with essential hypertension subdivided into three groups according to the WHO stage classification. The ratio of ejection time (ET) and pre-ejection period (PEP), ET/PEP remained within normal range in WHO-I but decreased significantly in WHO-II and reached extremely low values in WHO-III. ET did not change in WHO-I and WHO-II but became significantly reduced in WHO-III. Prolongation of PEP in WHO-II and WHO-III increased with progression of hypertensive stage. Isovolumic relaxation time (IRT) showed the same pattern as the prolongation of PEP; positive correlation between PEP and IRT was observed (r=0.55). On the other hand, significant changes of volumetric parameters were only observed in WHO-III. These results indicated that the time indices were a more sensitive parameter than the volumetric ones in the assessment of left ventricular dysfunction in the patients with essential hypertension.

Adult↗
PubMed1988

[Right ventricular dysfunction in demand-induced ischemia in patients with isolated right coronary artery disease: a radioisotope study].

In ischemic heart disease, the left ventricle has been considered the main target of an imbalance between myocardial oxygen supply and demand. Accordingly, the approach to ischemia has been directed at the evaluation of the left ventricle. The aim of this study was to assess the relative involvement of the left and right ventricle in patients with isolated right coronary artery stenosis. We studied 20 patients with a clinical history of effort angina (15 male, 5 female, mean age 54.1 +/- 6.2) using radionuclide angiography and atrial pacing. Findings were compared with those of 6 normal subjects that were paced at the maximal heart rate of 150 beats/min. Atrial pacing was interrupted because of diagnostic ST segment depression in 8 patients, Wenckebach type atrioventricular block in 1, chest pain without electrocardiographic changes in 4 and the achievement of the maximal prefixed heart rate of 150 beats/minute in 7. With respect to control conditions, during atrial pacing right ventricular ejection fraction declined from 46.8 +/- 6.8% to 37.4 +/- 8.1% (p less than 0.001), while no significant change was observed in left ventricular ejection fraction values (55.2 +/- 4.5% and 51.1 +/- 10.2% respectively). During atrial pacing, left ventricular peak filling rate increased from 1.77 +/- 0.53 to 4.71 +/- 1.8 end-diastolic volumes/second (p less than 0.0001). Qualitative analysis of regional wall motion showed a right ventricular dysfunction in 19/20 patients; this was prevalent in 9 and involving also the left ventricle in 10; an isolated impairment of the left ventricle was observed in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Contemporary medical management of left ventricular dysfunction and congestive heart failure.

OBJECTIVE: The primary purpose of this review was to address the following question: based on the best available evidence, what should be the current medical management of congestive heart failure (CHF)? DATA SOURCES: The major sources for this review were from searches of the English language literature, including computer and bibliography reviews, of all randomized, controlled clinical trials and overview analyses of positive inotropic agents, preload/afterload reduction agents and beta-blocker medications in CHF. STUDY SELECTION: The number of studies reviewed was approximately 40. The major criterion for selection was that the studies be of CHF patients in randomized controlled clinical trials, particularly with a mortality/survival endpoint. Additional clinical trials of nonmortality endpoints in CHF patients and mortality trials in non-CHF patients were also selected to support possible pathophysiological insights for future CHF trials. DATA EXTRACTION: The data, particularly for the accompanying tables, were initially extracted by a single reviewer using common qualitative guidelines as far as was possible within the different temporal, etiological and geographic frameworks of the original component studies. Conclusions are drawn from this data synthesis and from published overviews. DATA SYNTHESIS: Angiotensin converting enzyme (ACE) inhibition therapy is effective in reducing mortality and morbidity in severe left ventricular dysfunction and CHF. Other systemic vasodilators may also be beneficial. The effects of digitalis on survival and morbidity in CHF are presently uncertain, but should be resolved in the near future. Other inotropic agents, at least in the long term, are clinically detrimental. Diuretics decrease morbidity, but their effect on mortality in CHF remains unknown. Beta-blocker and magnesium therapy offer promise in CHF, but await definitive clinical trials evaluation. CONCLUSIONS: The current medical therapy of CHF should definitely include ACE inhibitors, probably diuretics and possibly other vasodilators. Further viable trials of promising new, and older heretofore under-evaluated, CHF therapies are needed. Additionally, innovative strategies are needed to deal with this disease which has an increasing prevalence. Two strategies, primary prevention of CHF and a 'Heart Function Clinic', are discussed.

Adrenergic beta-Antagonists↗
PubMed1997

Evaluation of plasma natriuretic peptides as markers for left ventricular dysfunction.

To test the hypothesis that elevated plasma levels of natriuretic peptides may serve to identify patients with left ventricular (LV) dysfunction, we assessed the predictive diagnostic value of natriuretic peptide levels, in addition to clinical and electro-cardiographic risk factors, as noninvasive indicators of cardiac dysfunction. Plasma levels of atrial natriuretic peptide (cANP) (99-126), N-terminal fragment of proANP (nANP) (26-55), nANP(80-96), brain natriuretic peptide (BNP-32), proBNP(22-46), and C-type natriuretic peptide (CNP-22) were measured in 211 subjects before cardiac catheterization. The strongest correlations with parameters of LV function were found for nANP(80-96) (up to r = -0.55, p < 0.0001), whereas there was no significant correlation with proBNP(22-46) or CNP-22. In patients with LV ejection fractions (LVEF) < or = 45% (n = 38) nANP(26-55), nANP(80-96), cANP(99-126), and BNP-32 were significantly increased (p < 0.001). Partition values for elevated versus normal natriuretic peptide levels were obtained from normal controls and used to separate subjects with and without LV dysfunction. Receiver operating characteristic analysis for LVEF < or = 45% indicated a significantly better diagnostic accuracy for high levels of nANP(80-96), nANP(22-56), cANP(99-126), and BNP-32 than for proBNP and CNP-22. Multivariate analysis by logistic regression identified Q waves and bundle branch block in the electrocardiogram as well as elevated plasma levels of cANP, nANP(80-96), and nANP(26-55) as the strongest independent predictors of low ejection fractions. The relative risk of LV dysfunction was raised up to tenfold in subjects with high natriuretic peptide levels (p < 0.001). The addition of nANP(80-96) and nANP(26-55) to the combination of clinical and electrocardiographic risk factors did not further improve the diagnostic sensitivity for the detection of LVEF < or = 45%, but it markedly increased the overall accuracy (59% to 81%, p < 0.001) and specificity (55% to 81%, p < 0.001). Among natriuretic peptides, elevated nANP(80-96) and nANP(26-55) levels have the strongest impact on the detection of LV dysfunction. They add to the diagnostic information contained in clinical and electrocardiographic factors. Plasma levels alone or in combination with clinical factors seem to be of value for a refined identification of abnormal LV function in the individual patient.

Aged↗
PubMed1983

Treatment of right ventricular dysfunction in acute respiratory failure.

The pathophysiology and managements of right ventricular (RV) dysfunction in acute respiratory failure (ARF) is complicated. Results presented in this paper indicate that volume expansion may not be appropriate therapy to maintain or increase cardiac output (CO) when flow is reduced because of increased RV afterload. Volume will increase RV wall stress and O2 requirements so that despite increased preload, CO may fall. If RV afterload is significantly increased, such changes can occur despite a relatively normal RV end-diastolic pressure (RVEDP). Further, increased RV afterload and/or volume expansion can result in increased RV volumes and secondary alteration in left ventricular (LV) diastolic mechanics. Such changes, especially if wedge pressure increases, would tend to increase pulmonary edema. Also, because of potential changes in viscosity and pulmonary vascular resistance (PVR), packed red blood cells may not be indicated to increase CO, arterial O2 content and tissue O2 delivery in the setting of ARF. Therapy designed to reduce PVR may be appropriate to increase flow in the setting of increased RV afterload. However, such therapy may also reduce systemic vascular resistance, blood pressure (BP) and RV perfusion pressure. Such changes could lead to RV ischemia and reduced CO. Alternatively, agents which increased RV perfusion and/or contractility will increase CO by reducing RV end-diastolic and end-systolic volumes and may be the treatment of choice to increase flow when RV afterload is elevated.

Aged↗
PubMed1993

Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors.

BACKGROUND: Left ventricular enlargement and the development of chronic heart failure are potent predictors of survival in patients after myocardial infarction. Prospective studies relating progressive ventricular enlargement in individual patients to global and regional cardiac dysfunction and the onset of late chronic heart failure are not available. It was the aim of this study to define the relation between left ventricular dilatation and global and regional cardiac dysfunction and to identify early predictors of enlargement and chronic heart failure in patients after myocardial infarction. METHODS AND RESULTS: Left ventricular volumes, regional area shrinkage fraction in 18 predefined sectors (gated single photon emission computed tomography), global ejection fraction, and hemodynamics at rest and during exercise (supine bicycle, 50 W, 4 minutes, Swan-Ganz catheter) were assessed prospectively 4 days, 4 weeks, 6 months, and 1.5 and 3 years after first myocardial infarction. Seventy patients were assigned to groups with progressive, limited, or no dilatation. Patients without dilatation (n = 38) maintained normal volumes and hemodynamics until 3 years. With limited dilatation (n = 18), left ventricular volume increased up to 4 weeks after infarction and stabilized thereafter; depressed stroke volume was restored 4 weeks after infarction and then remained stable at rest. Wedge pressure during exercise, however, progressively increased. With progressive dilatation (n = 14), depressed cardiac and stroke indexes were also restored by 4 weeks but progressively deteriorated thereafter. Area shrinkage fraction as an estimate of regional left ventricular function in normokinetic sectors at 4 days gradually deteriorated during 3 years, but hypokinetic and dyskinetic sectors remained unchanged. Global ejection fraction fell after 1.5 years, whereas right atrial pressure, wedge pressure, and systemic vascular resistance increased. By multivariate analysis, ejection fraction and stroke index at 4 days, ventriculographic infarct size, infarct location, and Thrombolysis in Myocardial Infarction trial grade of infarct artery perfusion were significant predictors of progressive ventricular enlargement and chronic dysfunction. CONCLUSIONS: Almost 26% of patients may develop limited left ventricular dilatation within 4 weeks after first infarction, which helps to restore cardiac index and stroke index at rest and to preserve exercise performance and therefore remains compensatory. A somewhat smaller group (20%) develops progressive structural left ventricular dilatation, which is compensatory at first, then progresses to noncompensatory dilatation, and finally results in severe global left ventricular dysfunction. In these patients, depression of global ejection fraction probably results from impairment of function of initially normally contracting myocardium. Early predictors from multivariate analysis allow identification of patients at high risk for progressive left ventricular dilatation and chronic ventricular dysfunction within 4 weeks after acute infarction.

Aged↗
PubMed1983

Assessment of left ventricular dysfunction by thallium-201 lung uptake during exercise in coronary artery disease.

To determine the clinical significance of an increased thallium-201 (Tl-201) activity in the lung and of its clearance from the lung after exercise, computer-quantitated Tl-201 lung activity was measured and compared with hemodynamic parameters at rest and during exercise in 35 patients with coronary artery disease (CAD). All patients underwent a supine bicycle ergometer exercise test and mean pulmonary artery wedge pressure (PAWP) was measured by a Swan-Ganz catheter. Coronary angiography was also performed. On computer-generated initial and 2 and a half hours delayed anterior images, regions of interest were selected over the myocardium (M) and lung (L), and the initial L/M ratio and the (initial L)/(delayed L) ratio were calculated as indices of an increased Tl-201 lung uptake and lung clearance, respectively. The initial L/M ratio and the (initial L)/(delayed L) ratio had no significant correlation with mean PAWP at rest and had a weak negative correlation with the resting ejection fraction (r = -0.57 and r = -0.58, respectively). However, both ratios showed good correlations with mean PAWP during peak exercise (r = 0.85 and r = 0.80, respectively), suggesting that they provide useful indices for assessing the severity of exercise-induced left ventricular dysfunction.

Adult↗
PubMed1981

Antihypertensive therapy with prazosin in patients with left ventricular dysfunction. Improvement in cardiac performance and exercise tolerance.

Although the relationship between blood pressure and cardiac performance has been widely recognized, there are few published clinical observations concerning the effect of blood pressure control on cardiac function. We evaluated the effect of prazosin, an antihypertensive agent which also improves hemodynamic measurements in normotensive patients with heart failure, in 16 patients with moderate hypertension and reduced ejection fractions. Therapy with digoxin and diuretics was continued throughout the study, but other antihypertensive agents were withdrawn at least one week prior to the initiation of the study. Measurements of ejection fraction, cardiothoracic ratio and the duration of maximal treadmill exercise were made before and after two months of antihypertensive therapy with prazosin. On prazosin, blood pressure fell from a mean of 169/103 to 141/84. Excellent control was achieved in 13/16 patients and significant reductions were noted in the remaining three. Concomitantly, ejection fraction rose from .38 +/- .02 (SEM) to .43 +/- .03 (P less than .02), cardiothoracic ratio decreased from .55 +/- .02 to .53 +/- .02 (P less than .05) and exercise capacity increased from 9.2 +/- 0.9 to 11.9 +/- 1.1 minutes (P less than .005). Prazosin was well tolerated except in one patient who experienced worsening angina. These findings emphasize the importance of rigorous blood pressure control in hypertensive patients with left ventricular dysfunction and indicate that prazosin is effective in this setting.

Aged↗
PubMed1984

Reflex constriction of significant coronary stenosis as a mechanism contributing to ischemic left ventricular dysfunction during isometric exercise.

To study the mechanisms of myocardial ischemia during isometric exercise, handgrip was sustained, for 4.5 min at 25% of maximum by 11 patients with at least one significant coronary stenosis each, during cardiac catheterization. After recovery, the handgrip that was repeated with simultaneous infusion of nitroglycerin (50 micrograms over 4 min) directly into the diseased vessel. The cardiovascular response was assessed by hemodynamic and by computer-assisted measurements of stenosis. During the first handgrip test pulmonary capillary wedge pressure rose 56% (15 to 23 mm Hg; p less than .001), the heart rate-systolic pressure product rose 33% (p less than .01), and the diseased epicardial arteries constricted. Luminal area in the stenotic segment was reduced by 35% (p less than .01), resulting in a 243% increase in estimated stenotic flow resistance (30 to 103 mm Hg/ml/sec; p less than .001). During handgrip with intracoronary nitroglycerin, the pressure-rate product again increased 33%, but relative to resting control, capillary wedge pressure fell 4 mm Hg in association with a 32% increase in luminal area of the stenosis and a 28% reduction in flow resistance (all significantly different from the response to handgrip alone: p less than .001, .01, and .005, respectively). Thus, coronary vasoconstriction, not increased pressure-rate product, is the dominant mechanism for ischemic left ventricular dysfunction during isometric exercise in patients with significant coronary stenoses.

Adult↗
PubMed1975

Right ventricular dysfunction detected by gated scintiphotography in patients with acute inferior myocardial infarction.

Twenty-seven patients with acute myocardial infarction not complicated by cardiogenic shock and ten normal volunteers were studied with gated cardiac blood pool scans. The ratio right vetricular area/left ventricular area (RVA/LVA) determined from the left anterior oblique end-diastolic scans was examined. The ratio was 1.11 +/- .06 in the normal volunteers. In patients with anterior infarction the ratio fell to 0.75 +/- .12 (P less than .05) due to left ventricular enlargement. In those with inferior infarction the ratio was 1.12 +/- .23 which was greater than in those with anterior infarction (P less than .05) due to enlargement of both the left and right ventricles. Six patients with cardiogenic shock, three with inferior and three with anterior infarction were studied. The three with anterior infarction had left ventricular enlargement and a decrease in the ratio of RVA/LVA to 0.62 while the three with inferior infarction had an increase in the ratio to 2.05 suggesting right ventricular dilatation and dysfunction. These studies suggest a high incidence of right ventricular dysfunction in patients with inferior myocardial infarction.

Aged↗
PubMed2003

Left ventricular dysfunction is associated with CD4 lymphocyte count rather than opportunistic infection in human immunodeficiency virus infection.

BACKGROUND AND PURPOSE: Left ventricular (LV) dysfunction is often found in the early stage of human immunodeficiency virus (HIV) infection and deteriorates with disease progression. CD4 lymphocyte count and opportunistic infection are the major indicators for the clinical staging of HIV infection. This study investigated the association of these indicators with LV dysfunction in the clinical course of HIV infection. METHODS: HIV-positive patients without cardiac manifestations consecutively admitted from May 1998 to April 1999 were enrolled in the study. Echocardiographic LV function evaluation and measurement of CD4 lymphocyte count were performed. Parameters for LV systolic and diastolic functions were compared between patients with CD4 lymphocyte count >or= 200/microL and those with CD4 < 200/microL. In patients with CD4 < 200/microL, LV function was further correlated with the presence or absence of opportunistic infections. RESULTS: Ninety eight HIV-positive patients including 52 with CD4 >or= 200/microL and 46 with CD4 < 200/microL were studied. One half of the 46 patients with CD4 < 200/microL had active opportunistic infections. We found that LV fractional shortening, ejection fraction, and isovolumic relaxation time were all significantly lower in the patients with CD4 < 200/microL compared with those with CD4 >or= 200/microL. Moreover, these LV systolic and diastolic dysfunctions were positively correlated with decreased CD4 lymphocyte count. In contrast, no difference was found in these parameters between patients with and without opportunistic infections. In multiple regression analysis, CD4 lymphocyte count was found to be the only factor for predicting the LV systolic and diastolic dysfunction. CONCLUSIONS: Both LV systolic and diastolic function deteriorate as the CD4 lymphocyte count decreases in HIV infection. Opportunistic infection seems to have a limited role in the pathogenesis of LV dysfunction in advanced HIV infection.

AIDS-Related Opportunistic Infections↗
PubMed1999

Right-sided pulsus alternans in diastolic left ventricular dysfunction.

Pulsus alternans is usually found in patients with reduced systolic ventricular function. We describe a patient with shortness of breath, hypertension, and left ventricular hypertrophy, but with normal left and right systolic function. Pulsus alternans was demonstrated in the pulmonary wedge position, pulmonary artery, and right ventricle, but not in the aorta or left ventricle. Cathet. Cardiovasc. Intervent. 47:336-339, 1999.

Diastole↗
PubMed2005

Left ventricular dysfunction after closure of large patent ductus arteriosus.

Changes in left ventricular dimensions and performance were studied in 43 patients after transcatheter occlusion or surgical ligation of patent ductus arteriosus. The patients were assigned to 2 groups based on their ductal diameter: >/= 3.1 mm to group A (n = 27) and </= 3 mm to group B (n = 16). The mean age and weight of the groups were comparable. Before intervention, group A had a significantly larger mean left ventricular end-diastolic diameter than group B, while all patients had normal shortening fraction and ejection fraction. Within 1 month after intervention, left ventricular end-diastolic diameter showed a trend towards regression while shortening fraction and ejection fraction decreased significantly in group A. There were no significant changes in these parameters in group B. Between 1 and 6 months after intervention, left ventricular performance improved in most of the group A patients who were followed up. We conclude that closure of large ductus arteriosus in children leads to significant immediate deterioration of left ventricular performance, which appears to recover within a few months. Echocardiographic study before hospital discharge is recommended in these patients. Serious deterioration of ventricular performance after closure may warrant the use of angiotensin converting enzyme inhibitors.

Cardiac Catheterization↗