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PubMed1994

Frequency of development of acute global left ventricular dysfunction in human immunodeficiency virus infection.

OBJECTIVES: This study evaluated prospectively the frequency, clinical outcome and pathologic findings of acute global left ventricular dysfunction in human immunodeficiency virus (HIV) infection during the various stages of the disease. BACKGROUND: Acute global left ventricular dysfunction in the course of HIV infection is still a poorly defined clinical entity, and little is known about the outcome after the acute onset. METHODS: Between January 1988 and June 1992, 136 HIV-positive (HIV+) patients without clinical, electrocardiographic or echocardiographic evidence of cardiovascular dysfunction on admission were prospectively studied with serial echocardiograms. Patients were assigned to three groups: 1) anti-HIV+ asymptomatic (17 patients, 12.5%); 2) acquired immunodeficiency syndrome (AIDS)-related complex (26 patients, 19.1%); 3) AIDS (93 patients, 68.4%). RESULTS: During a mean follow-up period of 415 +/- 220 days, seven patients, all in the AIDS subgroup, developed clinical and echocardiographic findings of acute global left ventricular dysfunction; of these, six (85%) died of congestive heart failure. Mean survival time from symptom onset was 41 +/- 13 days. Necropsy findings in five patients revealed acute lymphocytic myocarditis in three, cryptococcal myocarditis in one and interstitial edema and fibrosis in one. In only one patient was left ventricular dysfunction reversible with treatment. CONCLUSIONS: Although infrequent, acute global left ventricular dysfunction is not rare in the course of HIV infection. It seems to occur exclusively during the AIDS stage. Acute global left ventricular dysfunction is often fatal but may be reversible and is mainly associated with the pathologic findings of acute myocarditis.

AIDS-Related Complex↗

PubMedDate not supplied

Safety and feasibility of dobutamine-atropine stress echocardiography in patients with ischemic left ventricular dysfunction.

The aim of this study was to analyze whether left ventricular dysfunction affects the safety and feasibility of high-dose dobutamine-atropine stress echocardiography. We examined the results of the test in 318 consecutive patients who were referred for high-dose dobutamine-atropine stress echocardiography and also underwent diagnostic cardiac catheterization. Forty-four patients had a left ventricular ejection fraction of 25% or less (mean, 21%; range, 15% to 25%). In the entire group of 318 patients, no serious complications (death, myocardial infarction, or ventricular fibrillation) occurred. The overall feasibility of completing the test was excellent (97%). A trial fibrillation occurred in four patients, nonsustained ventricular tachycardia in 12, and sustained ventricular tachycardia in one. A decrease in systolic blood pressure of greater than 40 mm Hg or a peak systolic pressure of less than 80 mm Hg was present in eight cases. In the group with an ejection fraction of 25% or less, there was a higher rate of significant tachyarrhythmias (14% versus 5%; p = 0.03), whereas the feasibility of the test was slightly lower (89%; p < 0.01), but no difference for hypotension was found. By multivariate analysis, a history of tachyarrhythmias was the only predictor of stress-induced arrhythmias. Advanced left ventricular dysfunction does not represent a contraindication for dobutamine-atropine stress testing.

Adrenergic beta-Agonists↗

PubMed1996

Myocardial revascularization for severe left ventricular dysfunction. Factors influencing early and late survival.

The results of coronary bypass surgery have been assessed in 102 patients with severe left ventricular dysfunction who had a preoperative left ventricular ejection fraction of < or = 0.35 (mean (s.e.m.) 0.29 (0.01)). Independent risk factors influencing operative mortality were obesity (P = 0.0290) and the need for preoperative intra-aortic balloon counterpulsation (P = 0.0010). Cox regression analysis using as its end-point 'cardiac-related death' demonstrated three variables; the need for preoperative intra-aortic balloon counterpulsation (P < 0.001), advanced age (P = 0.011), and obesity (P = 0.36). In a subset of 43 patients who did not have these risk factors, the 4-year cardiac-related death rate was 95.1 (3.4)%. The operative mortality and long-term survival can be expected to be satisfactory in patients with severe left ventricular dysfunction, provided they have a viable myocardium rather than myocardial fibrosis.

Aged↗

PubMed1994

[What is the appropriate treatment for myocardial infarction with left ventricular dysfunction?].

The essential goal of medical treatment following myocardial infarction with left ventricular dysfunction must be the prevention of secondary cardiac failure. The existence of left ventricular dysfunction, in particular when it is not accompanied by clinical cardiac failure, is a virtually formal indication for beta-blocker treatment after an infarction. Beta-blockers with intrinsic sympathomimetic activity (ISA) are possibly better tolerated in this context. However, experience shows that cardiologists and general practitioners often remain reluctant to prescribe beta-blockers whenever left ventricular function is impaired. Converting enzyme inhibitors decrease the risk of onset of secondary cardiac failure, reduce sudden deaths by ventricular arrhythmias, reduce recurrences of myocardial infarction or unstable coronary insufficiency, and more generally reduce overall and cardiovascular mortality. This is a class effect. While there is no urgency to prescribe them during the acute phase, it is generally considered that it is extremely useful to give them fairly quickly, i.e. during the first 72 hours. At the end of the hospital phase, around two weeks, it is desirable, whenever possible, to prescribe a dose of the order of 75 mg/day of captopril or 2.5 mg/day of ramipril. The administration of aspirin can be considered virtually routine. Oral anticoagulants are desirable in the presence of a large akinetic pocket, a frequent starting point of thrombosis and/or systemic emboli, or in the presence of atrial fibrillation. Digitalis/diuretic treatment does not appear to be indicated at this stage. Other types of anti-ischemic treatment are not theoretically indicated as a matter of principle at this stage in the absence of residual ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed1994

Identification and revascularization of hibernating myocardium in angina-free patients with left ventricular dysfunction.

We examined 17 angina-free patients with left ventricular dysfunction, referred for surgical decision-making, who presented with no or few signs and symptoms of myocardial ischemia according to treadmill stress test. On cardiac catheterization they were affected by severe multi-vessel coronary artery disease; the mean left end-diastolic pressure of this population was 26.3 +/- 5.5 mm Hg (mean +/- SD) and their mean ejection fraction was 27.6 +/- 4.9% (mean +/- SD). They all were investigated for the presence of viable myocardium by the combined assessment of cardiac perfusion and metabolism using single photon emission tomography with [99mTc] labelled hexakis-2-methoxy-isobutyl-isonitrile [99mTc]MIBI/SPET) and positron emission tomography with [18F]-2-fluoro-2-deoxy-D-glucose ([18F]FDG/PET), respectively. Patients were considered for coronary surgery when [18F]FDG was detectable in at least two cardiac segments with wall motion abnormalities and perfusion defects. Nine patients were operated on, six were medically treated and two were scheduled for heart transplantation. We recorded no in-hospital mortality. At a mean follow-up of 28.4 +/- 9.8 (mean +/- SD) months all surgical patients were alive and their NYHA functional classes have improved, except in one case. Among the patients refused for bypass surgery, three are in stable conditions, three have worsened clinical statuses and two died while waiting for heart transplantation. In conclusion, for patients with bypassable coronaries, left ventricular dysfunction and lack of angina, successful coronary revascularization may be predicted by the presence of viable myocardium demonstrated with positron emission tomography.

Adult↗

PubMed1991

Studies of left ventricular dysfunction following myocardial infarction.

Early treatment of patients with myocardial infarction and left ventricular dysfunction was performed in 90 patients aiming at influencing left ventricular remodelling. After twelve months of treatment with 25 mg captopril t.i.d. left ventricular ejection fraction was improved by 10% in comparison to a treatment with 40 mg of frusemide or placebo (p = 0.001). Late treatment of the patients not treated with captopril resulted in partial reversal of left ventricular dilatation, while withdrawal of captopril therapy in stable patients with ejection fractions over 30% and without clinical signs of congestive heart failure did not result in deterioration of left ventricular function. These results give a sound rationale for the earlier use of ACE-inhibitors in the treatment of congestive heart failure and left ventricular dysfunction.

Captopril↗

PubMed1996

Role of basal release of nitric oxide in the presence of acute left ventricular dysfunction: comparative study with normal condition.

The basal release of nitric oxide (NO) plays an important role in the regulation of vascular circulation in the presence of acute left ventricular dysfunction. It is not clear, however, whether the role is as important in the presence of acute left ventricular dysfunction as it is in the normal condition. In addition, the effects of flow rate on the role of basal NO have not been clarified in the presence of acute left ventricular dysfunction. This in vivo study was attempted to compare the contribution of the basal release of NO to the regulation of vascular circulation and the effects of a mechanically reduced basal flow rate on the contribution of basally released NO between the normal condition and acute left ventricular dysfunction. In eight anesthetized dogs, the responses of femoral artery blood flow to NG-monomethyl-L-arginine (L-NMMA, 10(-5)M) were observed with and without a reduction in basal flow. The same observation was performed after the production of acute left ventricular dysfunction by coronary microembolization. Without the reduction in basal flow, the L-NMMA-induced decrease in femoral artery flow was significantly larger in acute left ventricular dysfunction than in the normal condition (-40 +/- 12% vs-17 +/- 6%, P < .01). Under the reduction in basal flow, there was no significant change in flow during the infusion of L-NMMA in the normal condition and only a small decrease in acute left ventricular dysfunction. There was no significant difference in the L-NMMA-induced changes in flow between these conditions. The contribution of basally released NO to the regulation of vascular circulation is larger in the presence of acute left ventricular dysfunction than in the normal condition; however, the role of basal NO is reduced with a decrease in basal flow rate.

Acetylcholine↗

PubMed1995

Clinical and therapeutic implications of chronic left ventricular dysfunction in coronary artery disease.

In patients with myocardial ischemia, left ventricular dysfunction (LV) may arise from irreversible damage (cell death), myocardial stunning (postischemic dysfunction), or myocardial hibernation (persistent myocardial dysfunction at rest due to underperfusion). Chronic LV dysfunction usually refers to hibernating myocardium. However, stunning might also become chronic, producing persistent myocardial dysfunction. Clinical studies have demonstrated that many patients with coronary artery disease have subsequent recurring ischemic (symptomatic or silent) episodes at short intervals in the same area and that each episode may be followed by myocardial stunning. In these patients the myocardium may not recover fully between episodes and function may remain reversibly depressed for long periods or may even be clinically depressed. The recognition of both stunning and hibernation is very important clinically and therapeutically, since chronic LV dysfunction may have a negative effect on mortality and morbidity in patients with coronary artery disease. Moreover, both clinical states are potentially correctable. Pharmacologic intervention with beta blockers, angiotensin-converting enzyme inhibitors, or calcium antagonists might improve or protect hibernating myocardium. The acute hemodynamic effects of the dihydropyridine calcium antagonist nisoldipine have been investigated in patients with chronic LV dysfunction probably arising from hibernating myocardium. Nisoldipine was found to improve both left ventricular systolic and diastolic function without activating the adrenergic system. The improvement in systolic function may be due to a redistribution of coronary blood flow and to a slight reduction in afterload induced by nisoldipine. On the other hand, nisoldipine may improve diastolic function in these patients by an intrinsic mechanism, Reducing intracellular calcium overload or balancing intracellular calcium homeostasis in the ischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗

PubMedDate not supplied

Left ventricular dysfunction and heart failure. Mechanistic and therapeutic distinctions.

Dysfunction of the left ventricle may result from a variety of insults, all of which may initiate a self-perpetuating process of ventricular remodeling which may progress to end-stage heart disease. Symptoms of heart failure may or may not co-exist with this ventricular remodeling. Treatment and prevention of these two largely distinct entities differ. Symptoms may respond to diuretics, vasodilators and digoxin. Progressive ventricular remodeling may be slowed by angiotensin converting enzyme inhibitors, hydralazine + isosorbide dinitrate and beta blockers. Prevention of symptomatic heart failure is dependent on early recognition of ventricular dysfunction and aggressive treatment to slow its progression. Development of more effective and targeted therapies will be dependent on expanded insight into the cellular and molecular mechanisms contributing to the remodeling process.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1983

Blood pressure and left ventricular dysfunction in the spontaneously hypertensive rat.

The important role of the heart in the manifestation of systemic hypertension often becomes apparent with the development of left ventricular dysfunction. After a prolonged course of stable compensated left ventricular hypertrophy, spontaneously hypertensive rats (SHR) developed left ventricular dysfunction. A phase of overt left ventricular dysfunction and dilatation was present at an advanced age (24 months) in female SHR, a phase during which systemic hypertension was no longer manifest despite the maintenance of an increased vascular resistance. Similarly, when left ventricular dysfunction was induced after the experimental production of a myocardial infarction, the systemic arterial pressure levels of young SHR fell. This reduction in blood pressure was directly related to the extent of the histologic damage to the left ventricle. These studies underscore the important permissive role of the heart in the expression and maintenance of systemic hypertension.

Aging↗

PubMed1986

Relation between left ventricular diastolic function and exercise tolerance in patients with left ventricular dysfunction.

Previous studies show no correlation between resting systolic left ventricular performance assessed as the ejection fraction and exercise tolerance. This study examined the relation between left ventricular diastolic performance and exercise tolerance in 63 patients with left ventricular dysfunction (ejection fraction less than 50%) due to known or suspected coronary artery disease. The 51 men and 12 women, aged 54 +/- 8 years (mean +/- standard deviation), underwent symptom-limited upright exercise testing on a bicycle ergometer. The exercise end-points were angina (n:5), dyspnea (n:16), and fatigue (n:42). The patients were divided into three groups: group 1 (n:28) with normal exercise tolerance (9.5 +/- 2.4 minutes), group 2 (n:18) with mild exercise intolerance (5.8 +/- 0.5 minutes), and group 3 (n:17) had severe exercise intolerance (3.7 +/- 0.9 minutes). The three groups did not differ in age, ejection fraction, end-diastolic volume, exercise end-point, exercise heart rate, and left ventricular peak filling rate at rest. The exercise peak filling rate was, however, significantly higher in group 1 (p = 0.03). Stepwise multivariate discriminant analysis of important variables identified the exercise peak filling rate as the only predictor of exercise tolerance (F = 6.0). Thus, variation in exercise peak filling rate may in part explain the variability of exercise tolerance in patients with left ventricular dysfunction; patients with preserved exercise capacity have higher exercise peak filling rate than those with exercise intolerance.

Adult↗

PubMed1994

Myocardial revascularization in patients with severe ischaemic left ventricular dysfunction: a clinical experience.

The benefits of myocardial revascularization in patients with ischaemic left ventricular dysfunction are widely reported. However, myocardial revascularization in such cases is associated with higher mortality and morbidity rates. Sixty patients with severe left ventricular dysfunction underwent myocardial revascularization at the authors' institution. Ejection fraction was assessed by angiocardioscintigraphy before and at 3 months after surgery. All patients underwent elective surgery and received complete myocardial revascularization. Myocardial protection was achieved using Buckberg's protocol. One perioperative death occurred. Weaning from cardiopulmonary bypass required inotropic drug therapy in 22 cases and aortic counterpulsation in nine. Perioperative myocardial infarction occurred in three patients with no further haemodynamic impairment. The mean postoperative ejection fraction was 41.0%, compared with a mean preoperative value of 26.5%. The extent of left ventricular functional improvement was greatest in those patients having the worst preoperative left ventricular function. It is concluded that, with this technique, myocardial revascularization can be achieved in patients with severe left ventricular dysfunction with an acceptable operative mortality.

Aged↗

PubMed1990

Silent left ventricular dysfunction during routine activity after thrombolytic therapy for acute myocardial infarction.

To investigate prospectively the occurrence and significance of postinfarction transient left ventricular dysfunction, 33 ambulatory patients who underwent thrombolytic therapy after myocardial infarction were monitored continuously for 187 +/- 56 min during normal activity with a radionuclide left ventricular function detector at the time of hospital discharge. Twelve patients demonstrated 19 episodes of transient left ventricular dysfunction (greater than 0.05 decrease in ejection fraction, lasting greater than or equal to 1 min), with no change in heart rate. Only two episodes in one patient were associated with chest pain and electrocardiographic changes. The baseline ejection fraction was 0.52 +/- 0.12 in patients with transient left ventricular dysfunction and 0.51 +/- 0.13 in patients without dysfunction (p = NS). At follow-up study (19.2 +/- 5.4 months), cardiac events (unstable angina, myocardial infarction or death) occurred in 8 of 12 patients with but in only 3 of 21 patients without transient left ventricular dysfunction (p less than 0.01). During submaximal supine bicycle exercise, only two patients demonstrated a decrease in ejection fraction greater than or equal to 0.05 at peak exercise; neither had a subsequent cardiac event. These data suggest that transient episodes of silent left ventricular dysfunction at hospital discharge in patients treated with thrombolysis after myocardial infarction are common and associated with a poor outcome. Continuous left ventricular function monitoring during normal activity may provide prognostic information not available from submaximal exercise test results.

Acute Disease↗

PubMed1994

Myocardial bioenergetic abnormalities in a canine model of left ventricular dysfunction.

OBJECTIVES: The purpose of this study was to assess high energy phosphate compound metabolism in remodeled left ventricular myocardium. BACKGROUND: The development of heart failure several years after myocardial infarction is often unexplained. Certain abnormalities of remodeled myocardium suggest that structural changes occurring in viable myocardium after discrete myocardial damage may contribute to the later appearance of heart failure. Whether these abnormalities alter metabolism in the surviving muscle and thereby possibly contribute to ventricular dysfunction is unknown. METHODS: High energy phosphate compound metabolism was assessed using spatially localized phosphorus-31 nuclear magnetic resonance spectroscopy. Eleven dogs with documented left ventricular dysfunction, resulting from infarction produced by transmyocardial direct current shock, were compared with eight normal dogs. Analyses were performed at baseline and during coronary hyperperfusion induced by intravenous adenosine. Myocardial blood flow was measured with radioactive microspheres. RESULTS: The creatine phosphate/adenosine triphosphate (CP/ATP) ratio was significantly reduced in the left ventricular dysfunction group in both the subepicardium ([mean +/- SE] 1.94 +/- 0.08 vs. 2.32 +/- 0.13, p = 0.019) and the subendocardium (1.71 +/- 0.07 vs. 2.05 +/- 0.07, p = 0.004). Intravenous adenosine produced significant coronary hyperemia in both groups but was less marked in dogs with left ventricular dysfunction. The improvement in myocardial perfusion was accompanied by a significant increase in the subendocardial CP/ATP ratio (from 1.71 +/- 0.07 to 1.92 +/- 0.08, p = 0.01) in dogs with left ventricular dysfunction. CONCLUSIONS: An abnormal transmural distribution of high energy phosphate compounds is evident in remodeled myocardium. This abnormality may be related in part to mismatch of oxygen delivery and demand.

Adenosine↗

PubMedDate not supplied

Influence of coronary artery disease and left ventricular dysfunction on postoperative mortality in vascular surgery.

In an attempt to assess the influence of coronary artery disease and left ventricular dysfunction on postoperative mortality, 107 patients consisting of 32 AAA resections and 44 aortoiliac and 31 femoropopliteal reconstructions were reviewed. All patients had a preoperative coronary angiograms and underwent cardiac catheterization to prevent cardiac-related deaths. Severe coronary artery disease was angiographically demonstrated in 40.6% of AAA, 31.8% of AI and 3.2% of FP patients. Severe left ventricular dysfunction was found in 21.9% of AAA, 18.2% of AI and 6.5% of FP. Both of the early and 5 (45.5%) of the 11 late deaths were caused by cardiac events. The nine-year survival rate (53.3%) in the patients with a documented combination of coronary artery disease and left ventricular dysfunction was significantly lower than those in patients with normal disease, normal left ventricular function and either documented coronary artery disease or left ventricular dysfunction. It is suggested from this series that left ventricular dysfunction is one of the most important risk factors in patients who undergo AAA resection and AI reconstruction and that severe disease and postoperative mortality are possibly reduced by certain kinds of interventional coronary therapies.

Actuarial Analysis↗

PubMed1996

Prognostic significance of plasma norepinephrine in patients with asymptomatic left ventricular dysfunction. SOLVD Investigators.

BACKGROUND: Elevated plasma neurohormonal levels are associated with increased mortality rates in patients with symptomatic heart failure. A previous Studies of Left Ventricular Dysfunction (SOLVD) trial suggested that neurohumoral activation precedes the development of symptoms as demonstrated by increased neurohormonal levels in patients with asymptomatic left ventricular dysfunction. However, the significance of this early neurohumoral activation is unclear. The goals of this study were to determine the prognostic significance of the plasma concentrations of plasma norepinephrine (PNE) and atrial natriuretic peptide (ANP) and the renin activity (PRA) in patients with asymptomatic left ventricular dysfunction. METHODS AND RESULTS: PNE and PRA were measured before randomization in 514 patients with left ventricular ejection fractions < or = 35% who did not require treatment for congestive heart failure and were enrolled in the SOLVD Prevention Trial. Plasma ANP levels were measured in a subset of 241 patients owing to study design. Using the Cox proportional hazards model that included left ventricular ejection fraction, New York Heart Association functional class, age, sex, treatment assignment to placebo or enalapril, and cause of heart failure, we examined whether these neurohormones predicted all-cause mortality, cardiovascular mortality, hospitalization for heart failure, development of heart failure, or development of ischemic events (myocardial infarction or unstable angina). PNE was the strongest predictor of clinical events in this patient population. PNE levels above the median of 393 pg/mL were associated with a relative risk of 2.59 (P = .002) for all-cause mortality, 2.55 (P = .003) for cardiovascular mortality, 2.55 (P = .005) for hospitalization for heart failure, 1.88 (P = .002) for development of heart failure, 1.92 (P = .001) for ischemic events, and 2.59 (P = .005) for myocardial infarction. PNE remained the most powerful predictor for all-cause mortality and ischemic events when the analysis included only the patients with histories of ischemic left ventricular dysfunction. The increases in other neurohormonal levels were not useful in predicting the subsequent development of clinical events. CONCLUSIONS: Increased PNE levels in patients with asymptomatic left ventricular dysfunction appear to predict all-cause and cardiovascular mortalities and development of clinical events related to the onset of heart failure or acute ischemic syndromes. Thus, measurement of PNE may be a possible early marker for assessment of disease progression in patients with left ventricular dysfunction, and modulating the release or effect of PNE may lead to improved prognosis and/or a reduction in morbidity.

Angina, Unstable↗

PubMed1995

Ergometric exercise testing and sensitivity of cyclic guanosine 3',5'-monophosphate (cGMP) in diagnosing asymptomatic left ventricular dysfunction.

OBJECTIVE: Increased plasma concentrations of cyclic guanosine monophosphate (cGMP) have been reported in patients with manifest heart failure. At rest, however, cGMP concentrations in patients with asymptomatic left ventricular dysfunction or heart failure in New York Heart Association (NYHA) functional class I do not differ significantly from those of healthy subjects. The purpose of this study was to investigate whether graded exercise on an ergometer improves the sensitivity of cGMP in diagnosing asymptomatic left ventricular dysfunction. PATIENTS: Plasma cGMP concentrations were compared in 17 healthy controls and 98 patients with asymptomatic left ventricular dysfunction or congestive heart failure of different stages (asymptomatic left ventricular dysfunction or NYHA functional class I, 56 patients; NYHA class II, 31 patients; NYHA class III, 11 patients). RESULTS: Before exercise plasma cGMP concentrations in patients with clinical heart failure (NYHA functional classes II and III) were significantly higher than those in healthy controls. In patients with asymptomatic left ventricular dysfunction or heart failure of functional class I plasma cGMP concentrations were not significantly different from those in healthy subjects. Thirty minutes after exercise, however, cGMP concentrations in patients with asymptomatic left ventricular dysfunction or class I heart failure were significantly higher than those in healthy controls. CONCLUSION: Measurement of plasma cGMP concentrations 30 minutes after ergometric exercise testing allows better discrimination between healthy subjects and patients with symptomless left ventricular dysfunction or mild heart failure (NYHA class I) than measurement of such concentrations before exercise.

Adult↗

PubMed1991

[The effects of coronary revascularization in patients with severe left ventricular dysfunction].

To evaluate the operative risk of coronary diseased patients who had severe left ventricular dysfunction, we retrospectively reviewed the cases of 798 patients who had received A-C bypass surgery at Juntendo University between Jan. 1984 and Dec. 1989. The patients with severe left ventricular dysfunction (Ejection Fraction less than 30%) (Group-A, n = 9) were compared with the patients with moderately impaired left ventricular function (E.F. 30%-40%) (Group-B, n = 28) and normal left ventricular function (E.F. greater than or equal to 50%) (Group C, n = 34). The mean E.F. were 21.56 +/- 3.72% in Group-A, 34.28 +/- 3.17% in Group-B, 64.19 +/- 12.02% in Group-C. There were no differences between the 3 groups with regard to Cardiac Index, LVEDP, number of diseased vessels, number of grafts, aortic cross clamp time and cardio-pulmonary bypass time. The percentages of patient who needed catecholamines support in postoperatively were 77.8% in Group-A, 46.4% in Group-B and 61.8% in Group-C. There were no operative and hospital deaths in each of the 3 Groups, whereas 2 patients of Group-A died later of noncardiac disease. We propose that patients with severe left ventricular dysfunction (15 less than or equal to EF, less than 30%) benefit from CABG surgery with low risk, and that each left ventricular E.F., Cardiac Index or LVEDP alone were less significant predictors of operative results as measured by preoperative left ventricular function.

Adult↗