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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↗

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↗

Comparison of functional recovery of mildly hypokinetic versus severely dysfunctional left ventricular segments after revascularization in patients with ischemic cardiomyopathy.

Dysfunctional left ventricular (LV) segments showing contractile reserve during dobutamine stress echocardiography (DSE) are considered viable myocardium; functional recovery is expected after revascularization. Many segments, however, particularly mildly hypokinetic segments, do not recover. The reason for this failure is unknown. Two-dimensional echocardiography at rest and low-high-dose DSE were performed before revascularization in 114 consecutive patients with ischemic cardiomyopathy. Two-dimensional echocardiography at rest was repeated after 9 to 12 months. Segmental function was scored by a 5-point grading score. Functional recovery after revascularization was assessed in mildly hypokinetic (score 2, group I) and severely dysfunctional segments (score 3 to 5, group II). For each segment, functional recovery was defined as an improvement in functional score of > or =1 grade compared with the baseline score at rest. During low-dose DSE (up to 10 microg/kg/min), 183 group I segments (68%) and 438 group II (39%) segments had contractile reserve (p <0.0001). However, functional recovery was observed less frequently in group I segments (41%) than in group II segments (55%) with contractile reserve (p <0.005). During high-dose DSE (up to 40 microg/kg/min), in the group I segments with contractile reserve at the low dose, the sustained improvement pattern (indicating subendocardial scar) was prevalent (73%). After revascularization, 73% of segments with sustained improvement did not recover. Conversely, the biphasic response (indicating ischemically jeopardized myocardium) was observed only in 27% of group I segments. Functional recovery occurred in 39 of these segments (78%) (p <0.001 vs sustained improvement). Hence, mildly hypokinetic segments probably indicate the presence of subendocardial scars, and may explain the failure in functional recovery after revascularization.

Adult↗

Use of the peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage.

OBJECT: Differentiating myocardial infarction (MI) from reversible neurogenic left ventricular dysfunction (stunned myocardium [SM]) associated with aneurysmal subarachnoid hemorrhage (SAH) is critical for early surgical intervention. The authors hypothesized that the cardiac troponin (cTn) trend and/or echocardiogram could be used to differentiate between the two entities. METHODS: A retrospective study was conducted for the period between 1995 and 2000. All patients included in the study met the following criteria: 1) no history of cardiac problems; 2) new onset of abnormal cardiac function (ejection fraction [EF] < 40% on echocardiograms); 3) serial cardiac markers (cTn and creatine kinase MB isoform [CK-MB]); 4) surgical intervention for their aneurysm; and 5) cardiac output monitoring either by repeated echocardiograms or invasive hemodynamic monitoring during the first 4 days post-SAH when the patients were euvolemic. Of the 350 patients with SAH, 10 (2.9%) had severe cardiac dysfunction. Of those 10, six were women and four were men. The patients' mean age was 53.5 years (range 29-75 years) and their SAH was classified as Hunt and Hess Grade III or IV. Aneurysm distribution was as follows: basilar artery tip (four); anterior communicating artery (two); middle cerebral artery (one); posterior communicating artery (two); and posterior inferior cerebellar artery (one). The mean EFonset was 33%. The changes on echocardiograms in these patients did not match the findings on electrocardiograms (EKGs). Within 4.5 days, dramatic improvement was seen in cardiac output (from 4.93 +/- 1.16 L/minute to 7.74 +/- 0.88 L/minute). Compared with historical controls in whom there were similar levels of left ventricular dysfunction after MI, there was no difference in peak CK-MB. A 10-fold difference, however, was noted in cTn values (0.22 +/- 0.25 ng/ml; control 2.8 ng/ml; p < 0.001). CONCLUSIONS: The authors determined the following: 1) that the CK-MB trend does not allow differentiation between SM and MI; 2) that echocardiograms revealing significant inconsistencies with EKGs are indicative of SM; and 3) that cTn values less than 2.8 ng/ml in patients with EFs less than 40% are consistent with SM.

Adult↗

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↗

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↗

Results of revascularization in patients with severe left ventricular dysfunction.

OBJECTIVE: In patients with coronary disease and poor left ventricular function, bypass grafting remains a surgical challenge. This study evaluates experience in 125 consecutive patients with ejection fraction less than 20% (study group). METHODS: Preoperative viability studies were not used for patient selection. Clinical data were prospectively collected. The average age of the study subjects was 59 +/- 9 years, and 112 (90%) were male. Most patients (108 [86%]) were in symptom class III or IV. Main indications for surgery included angina in 62 (50%), heart failure and angina in 36 (29%), heart failure in 9 (7%), ventricular arrhythmia in 2 (2%), and critical anatomy in 16 (13%). Significant mitral regurgitation was present in 48 (38%), and distal vessels were poorly visualized in 67 (54%). At surgery, temperature mapping guided an integrated approach to cold cardioplegia. Results in this group were compared with those obtained in case-matched control subjects receiving cardioplegia without temperature mapping (matched for age, sex, functional class, and urgency of operation). RESULTS: Hospital morbidity (intra-aortic balloon pump support) and mortality rates were significantly lower in the study group versus those of control subjects (15% vs 30%, P =. 004; and 4% vs 11%, P =.03, respectively). In study patients the 5-year actuarial survival was 72%. Among survivors, both anginal class and heart failure class improved significantly. By means of multivariate analysis, survival was adversely affected by older age, class IV symptoms, and poorly visualized distal vessels. CONCLUSIONS: These results support the use of coronary artery bypass grafting in patients with severe left ventricular dysfunction without case selection on the basis of viability studies or visibility of distal vessels. Low hospital morbidity and mortality rates have been achieved when temperature mapping guides cardioplegia. Symptoms are improved in most patients, and long-term survival is encouraging.

Case-Control Studies↗

Differential coronary microvascular function in patients with left ventricular dysfunction of unknown cause--implication for possible mechanism of myocardial ischemia in early stage of cardiomyopathy.

To evaluate whether or not coronary microvascular dysfunction is associated with exercise-induced myocardial ischemia in left ventricular dysfunction of unknown cause, both the treadmill exercise test (TET) and coronary hemodynamics were studied in 20 patients with impaired left ventricular ejection fraction (<50% by radionuclide ventriculogram), normal cardiac size, normal coronary angiogram and no evidence of clinical heart failure. Ten subjects with atypical chest pain were studied as the control. Coronary hemodynamics were studied both at baseline and after dipyridamole infusion (0.56mg/kg, i.v. for 4'). There was no difference in age, gender, blood pressure, baseline great cardiac venous flow (GCVF) and coronary vascular resistance between ten patients with a positive TET and the other ten with a negative TET. At baseline, coronary sinus oxygen concentration was increased and myocardial oxygen consumption reduced in patients with a positive TET compared with those with negative a TET. After dipyridamole infusion, maximum GCVF (102+/-47 vs. 144+/-31 ml/min, P=0.027) and coronary flow reserve (2.31+/-0.49 vs. 3.00+/-0.61, P=0.012) were significantly reduced and minimum coronary vascular resistance was higher (1.00+/-0.42 vs. 0.63+/-0.12 mmHg/ml/min, P=0.016) in patients with a positive TET than in those with a negative TET. At follow-up, 40% of patients with a positive TET and 10% of those with a negative TET developed clinical heart failure with a dilated left ventricle during a period of 45 months. Thus, coronary microvascular function is heterogeneous in patients with left ventricular dysfunction of unknown cause. In some of them, coronary microvascular dysfunction could be related to the presence of exercise-induced myocardial ischemia, suggesting that similar pathophysiology underlies the early stage of dilated cardiomyopathy and syndrome X.

Adult↗

Multiple episodes of a transient global left ventricular dysfunction reminiscent to apical ballooning.

A new cardiac syndrome with transient left ventricular dysfunction has been recently reported and is referred to as Tako-Tsubo cardiomyopathy, which is characterized by a transient akinesia of the apex and compensatory basal hyperkinesis. Today, the etiology remains unknown. We report for the first time of a patient with multiple episodes of a transient global left ventricular dysfunction which is reminiscent to apical ballooning. These episodes were always preceded by severe emotional stress proposing a potential common pathomechanism.

Cardiomyopathies↗

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↗

Long-term outcome after coronary artery bypass grafting in patients with severe left ventricular dysfunction.

BACKGROUND: The aim of this study was to define the potential for long-term survival with severe left ventricular dysfunction after coronary bypass and to quantify any improvement in overall functional status. METHODS: Left ventricular dysfunction was confirmed preoperatively and the long-term survival and functional outcome after bypass was determined by follow-up studies obtained during the span of a decade. RESULTS: From 1/1990 to 12/1999, 86 patients with severe left ventricular dysfunction (mean ejection fraction, 0.18 +/- 0.03; range, 0.10 to 0.20) underwent coronary artery bypass grafting. There were 10 perioperative deaths (11% mortality). The mean survival was 55 months (standard deviation +/- 34 months; range, 2 to 141 months) with an actual 5-year survival rate of 59% (actuarial 5-year 65%, 10-year 33%). Echocardiography obtained between 1 and 6 months, 6 months and 1 year, 1 and 2 years, 2 and 4 years, 4 and 6 years, and 6 and 11 years showed the ejection fraction improved to 0.29 +/- 0.08 (p < 0.001), 0.31 +/- 0.14 (p < 0.002), 0.35 +/- 0.08 (p < 0.001), 0.27 +/- 0.10 (p = 0.002), 0.36 +/- 0.14 (p = 0.004), and 0.30 +/- 0.11 (p = 0.004), respectively. At 1 to 6 months, 6 months to 1 year, and 1 to 2 years, the diastolic left ventricular dimension was unchanged, but the systolic left ventricular dimension decreased significantly from 5.02 +/- 0.77 cm to 4.26 +/- 0.91 cm (p = 0.046), 3.98 +/- 1.43 cm (p = 0.08), and 4.10 +/- 1.14 cm (p = 0.07). The preoperative New York Heart Association classification for all patients improved from 2.8 +/- 0.8 to 1.6 +/- 0.7 (p < 0.001) after a mean of 53 months (standard deviation +/- 34 months). CONCLUSIONS: Patients with severe left ventricular dysfunction can derive long-term benefit from coronary bypass through improved left ventricular contractility as documented by a significantly decreased systolic left ventricular dimension and increased ejection fraction. Successful bypass is associated with a 59% actual 5-year survival rate and significantly improved New York Heart Association functional class.

Actuarial Analysis↗

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↗

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↗

The semi-elective use of the pulmonary artery flotation catheter in children with progressive pulmonary hypertension or left ventricular dysfunction.

OBJECTIVE: To describe the experience with the semi-elective use of the pulmonary artery flotation catheter in pediatric patients with progressive pulmonary hypertension or left ventricular dysfunction. DESIGN: Prospective study. SETTING: Pediatric intensive care unit in a tertiary care center. PATIENTS: Seven consecutive children with pulmonary hypertension and ten children with left ventricular dysfunction. INTERVENTIONS: Drug-response studies were performed using a pulmonary artery flotation catheter. Cardiac index, systemic and pulmonary blood pressure, and occlusion pressure were measured during incremental doses of calcium channel blocker (diltiazem) that were administered to children with pulmonary hypertension and during incremental doses of nitroglycerine and angiotensin-converting enzyme-inhibitor (captopril) that were administered to patients with left ventricular dysfunction. MAIN RESULTS: Four patients (60%) with pulmonary hypertension were identified as responders to calcium channel blockers, resulting in maintenance therapy with high-dose diltiazem in three of them. Nine patients (90%) with left ventricular dysfunction showed a >15% increase in cardiac index with vasodilator therapy. Eleven patients (65%) developed fever during the procedure. Nine patients (53%) had a high probability of bacterial infection. Seven patients (40%) died within 3.5 months after the procedure. Fever, infection, and mortality appeared to occur more frequently in patients in New York Heart Association classes III and IV. CONCLUSIONS: The use of a pulmonary artery flotation catheter enables us to optimize medical treatment strategies in the individual child with progressive pulmonary hypertension or left ventricular dysfunction. Children with left ventricular dysfunction in poor clinical condition showed a high mortality rate post or propter the procedure. In our opinion, drug-response studies using pulmonary artery flotation catheters in patients with left ventricular dysfunction should be performed in a relatively early stage of the disease.

Journal Article↗

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↗

Assessment of synchronized direct mechanical ventricular actuation in a canine model of left ventricular dysfunction.

Direct mechanical ventricular actuation (DMVA) is an experimental procedure that provides biventricular cardiac assistance by intracorporeal pneumatic compression of the heart. The advantages this technique has over other assist devices are biventricular assistance, no direct blood contact, pulsatile blood flow, and rapid, less complicated application. Prior studies of nonsynchronized DMVA support have demonstrated that a subject can be maintained for up to 7 days. The purpose of this study was to determine the acute hemodynamic effects of cardiac synchronized, partial DMVA support in a canine model (RVP) of left ventricular (LV) dysfunction. The study consisted of rapidly pacing seven dogs for 4 weeks to create LV dysfunction. At the conclusion of the pacing period, the DMVA device was positioned around the heart by means of a median sternotomy. The animals were then imaged in a 1.5 T whole body high speed clinical MR system, with simultaneous LV pressure recording. Left ventricular pressure-volume (PV) loops of the nonassisted and DMVA assisted heart were generated and demonstrated that DMVA assist shifted the loops leftward. In addition, assist significantly improved pressure dependent LV systolic parameters (left ventricular peak pressure and dp/dt max, p < 0.05), with no diastolic impairment. This study demonstrates that DMVA can provide synchronized partial assist, resulting in a decrease in the workload of the native heart, thus having a potential application for heart failure patients.

Animals↗

New positive inotropic agents in the treatment of left ventricular dysfunction.

Three major classes of inotropic agents have been clinically evaluated in patients with left ventricular dysfunction: a) agents that increase the intracellular concentration of cyclic adenosine monophosphate by stimulating the beta-adrenergic receptor or inhibiting phosphodiesterase; b) drugs that increase the intracellular sodium concentration; c) the new calcium-sensitizing drugs. This review will focus on the newest drug for each of the above-mentioned classes of inotropic agents. Moreover, we present a new protocol which provides the use of levosimendan in patients with post-ischemic left ventricular dysfunction.

Cardiotonic Agents↗

Risk stratification of patients with coronary artery disease and left ventricular dysfunction by exercise radionuclide angiography and exercise electrocardiography.

BACKGROUND: The results of multicenter trials indicate that patients with left ventricular dysfunction and either three-vessel or left main coronary artery disease have improved prognosis when treated surgically. OBJECTIVE: As part of a larger evaluation and follow-up study of coronary artery disease, the objective of this investigation was to determine whether exercise radionuclide angiography can be used, in patients with mild symptoms of coronary artery disease and left ventricular dysfunction at rest, to identify patients with three-vessel or left main coronary artery disease. METHODS AND RESULTS: Eighty-four consecutive patients were studied with angiographically defined coronary artery disease in whom left ventricular ejection fraction at rest ranged from 20% to 40%. Patients underwent exercise electrocardiography, rest and exercise radionuclide angiography, and 24-hour electrocardiographic monitoring. There were 22 patients with one-vessel, 31 with two-vessel, 27 with three-vessel, and four with left main coronary artery disease. All but four patients had a documented history of myocardial infarction. By univariate analysis, the following parameters were related to the anatomic severity of coronary artery disease: magnitude of ST segment depression with exercise (p < 0.001), magnitude of change in ejection fraction with exercise (p < 0.005), and occurrence of angina during exercise (p < 0.005). However, because of the extensive overlap among anatomic subgroups, no single factor had both a satisfactory sensitivity and a satisfactory specificity in identifying patients with three-vessel and left main coronary artery disease. Multivariate stepwise regression analysis also failed to predict three-vessel or left main coronary artery disease satisfactorily (sensitivity 73% and specificity 73%; positive predictive accuracy 59% and negative predictive accuracy 83%). Nonetheless, this multivariate analysis provided important prognostic information. During medical therapy (mean follow-up 56 months), the patients with a high likelihood of three-vessel or left main coronary artery disease had a greater risk of death or reinfarction than had patients with a low likelihood (p < 0.05). These functional data were better than coronary anatomy alone in providing risk stratification. Four of six patients with two-vessel disease who died were classified incorrectly by the multivariate analysis in the high-likelihood group for three-vessel or left main coronary artery disease, but classified correctly as being at high risk; whereas none of the patients with three-vessel disease who were misclassified in the low-likelihood group died during medical therapy. CONCLUSION: Although exercise radionuclide angiography in patients with minimal symptoms of coronary artery disease and left ventricular dysfunction is not precise in predicting three-vessel or left main coronary artery disease, it provides important functional information regarding subsequent prognosis during medical therapy.

Adult↗