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PubMed1994

Left ventricular dysfunction due to stunning and hibernation in patients.

Left ventricular dysfunction is in most cases the consequence of myocardial ischemia. It may occur transiently during an attack of angina and usually it is reversible. It may persist over hours or even days in patients after an episode of ischemia followed by reperfusion, leading to the so-called condition of stunning. In patients with persistent limitation of coronary flow, left ventricular dysfunction may be present over months and years, or indefinitely in subjects with fibrosis, scar formation, and remodeling after myocardial infarction. However, chronic left ventricular dysfunction does not mean permanent or irreversible cell damage. Hypoperfused myocytes can remain viable but akinetic. This type of dysfunction has been called hibernating myocardium. The dysfunction due to hibernation can be partially or completely restored to normal by reperfusion. It is, therefore, important to clinically recognize a hibernating myocardium. In the present article we evaluate stunning and hibernation with respect to clinical decision making and, when possible, we refer to our ongoing clinical experience.

Humans↗
PubMed1990

Effect of inotropic and vasodilator therapy on left ventricular diastolic filling in dogs with severe left ventricular dysfunction.

Inotropic and vasodilator therapy for congestive heart failure improve left ventricular systolic performance by different mechanisms. However, the nature and extent to which diastolic filling is altered have not been well described. Acute severe left ventricular dysfunction was induced in 21 dogs by severe left ventricular global ischemia produced by left main coronary artery microsphere embolization until left ventricular end-diastolic pressure was greater than or equal to 18 mm Hg. Dobutamine was infused in seven dogs until the peak positive first derivative of left ventricular pressure (dP/dt) increased by greater than or equal to 33%. Nitroprusside was infused in seven dogs until left ventricular end-diastolic pressure was less than 15 mm Hg. Seven dogs were observed for 1 h after the induction of acute severe left ventricular dysfunction and served as the control group. In all groups of dogs, severe left ventricular dysfunction resulted in left ventricular dilation, reduction in area ejection fraction, elevation of left ventricular end-diastolic pressure and an early redistribution of diastolic filling (increased 1/3 and 1/2 filling fractions) despite a markedly abnormal time constant of relaxation. No changes were noted in any variable after 1 h of observation in the seven control dogs. Nitroprusside reduced left ventricular size and filling pressure, increased cardiac output, improved relaxation and redistributed diastolic filling to later in diastole as characterized by a reduced 1/3 filling fraction (19.4 +/- 7.4% versus 51.4 +/- 10%, p less than 0.001). The pressure-area curve was shifted downward and leftward.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Reversal of left ventricular dysfunction after renal transplantation.

We report the cases of four patients with end-stage renal disease and New York Heart Association class III or IV heart failure of nonischemic origin as documented by coronary angiography. Because of left ventricular dysfunction (left ventricular end-diastolic pressure, 23 to 30 mm Hg; ejection fraction, 20% to 35%), all four patients were initially considered poor surgical candidates for renal transplantation. These same four patients became asymptomatic, however, with markedly improved cardiac function (ejection fraction, 43% to 69%) detected as early as 6 and 14 days after renal engraftment. Therefore, there exists a subset of patients with end-stage renal disease in whom congestive heart failure should not be considered a contraindication to renal transplantation. We conclude that some dialysis-dependent patients who manifest symptomatic heart failure of nonischemic origin have a reversible cardiomyopathy and should not be denied renal transplantation.

Adult↗
PubMed1994

Detection of left ventricular dysfunction after acute myocardial infarction: comparison of clinical, echocardiographic, and neurohormonal methods.

OBJECTIVE: The SAVE study showed that captopril improves mortality in patients with left ventricular dysfunction after myocardial infarction and that this benefit occurred even in patients with no clinically overt heart failure. On the basis of this, it seems important to identify correctly which patients have left ventricular dysfunction after a myocardial infarction. The objective was to compare various methods of identifying patients with left ventricular dysfunction (left ventricular ejection fraction, LVEF, < or = 40%) after acute myocardial infarction. The methods compared were echocardiography (quantitative and qualitative visual assessment), clinical evaluation (subjective assessment and three clinical score methods), and measurement of plasma concentrations of cardiac natriuretic peptide hormones (atrial and brain natriuretic peptides, ANP and BNP). DESIGN: Cross sectional study of left ventricular function in patients two to eight days after acute myocardial infarction. SETTING: Coronary care unit of a teaching hospital. PATIENTS: 75 survivors of a recent myocardial infarction aged 40 to 88 with no history of cardiac failure and without cardiogenic shock at the time of entry to the study. MAIN OUTCOME MEASURES: Sensitivities and specificities of the various methods of detecting left ventricular dysfunction were calculated by comparing them with a cross sectional echocardiographic algorithm for LVEF. RESULTS: Clinical impression was poor at identifying LVEF < 40% (sensitivity 46%). Clinical scoring improved this figure somewhat (modified Peel index sensitivity 64%). Qualitative visual assessment echocardiography was a more sensitive method (sensitivity 82%) for detecting LVEF < 40%. Plasma BNP concentration was also a sensitive measure for detecting left ventricular dysfunction (sensitivity 84%) but plasma ANP concentration was much poorer (sensitivity 64%). CONCLUSION: Left ventricular dysfunction is easily and reliably detected by echocardiographic measurement of LVEF and also by a quick qualitative echocardiographic assessment but is likely to be missed by clinical assessment alone. High concentrations of plasma BNP maybe another useful indicator of left ventricular dysfunction, particularly in hospitals where not all patients can be screened by echocardiography or radionuclide ventriculography after myocardial infarction.

Adult↗
PubMed1982

Normal exercise capacity in patients with severe left ventricular dysfunction: compensatory mechanisms.

About one-third of patients who have severe left ventricular dysfunction can achieve normal levels of exercise. To elucidate the mechanisms that permit this to occur, we studied six patients with severe left ventricular dysfunction (average left ventricular ejection fraction 17 +/- 2.5% [mean +/- SEM]) who achieved nearly normal levels of exercise tolerance (greater than 11 minutes of treadmill exercise, Sheffield protocol). All patients had normal pulmonary function at rest and during exercise. Hemodynamics were measured at rest and during supine and upright exercise. The major mechanisms of the preserved exercise capacity in these patients were chronotropic competence, ability to tolerate elevated wedge pressures (33 +/- 3 mm Hg) without dyspnea, ventricular dilation, and increased levels of plasma norepinephrine at rest and during exercise. Also, whereas peripheral vascular resistance was unchanged during supine exercise, it decreased by 50% during similar levels of upright exercise. As a consequence, increases in cardiac output from rest to exercise were greater during upright than supine exercise (100% vs 50%, respectively) (p less than 0.05), and pulmonary wedge pressures were lower during upright than supine exercise (21 +/- 5 mm Hg vs 33 +/- 3 mm Hg). Thus, multiple mechanisms permit some patients with severe left ventricular dysfunction to achieve normal levels of exercise. These studies emphasize that left ventricular function must be assessed by direct means rather than inferring function of the left ventricle from the results of an exercise tolerance test.

Aged↗
PubMed1993

Calcium antagonists or beta-blockers in chronic ischaemic left ventricular dysfunction?

Angina pectoris in patients with severe left ventricular dysfunction (LVD), with or without heart failure, is important clinically and socioeconomically. In the Studies of Left Ventricular Dysfunction (SOLVD), more than 36% of the patients had angina pectoris. Although angiotensin-converting enzyme (ACE) inhibitors improve survival and reduce the incidence of new, acute ischaemic events in these patients, they have no significant impact on the incidence of anginal attacks. Treatment of these patients must, therefore, primarily rely on nitrates, beta-blockers and calcium channel blockers. The beta-blockers, by lowering heart rate, improve the balance between myocardial oxygen supply and demand during exercise, and are among the most effective anti-anginal agents available. In addition, by reducing resting heart rate and by preventing excessive catecholamine stimulation of the myocardium, beta-blockers may slow the progression of ischaemic LVD. This may contribute to the improved survival observed when these agents are used following myocardial infarction. By reducing cardiac sympathetic stimulation, however, beta-blockers may depress right and left ventricular pump function. This depression is generally of no clinical consequence when the ejection fraction remains above 40%, but when the ejection fraction is below 35%, only 30% of patients without heart failure and 10% of those with heart failure seem to tolerate a full dose of beta-blocker. This limits their therapeutic use in angina in this setting. Moreover, beta-blockers do not act on the mechanisms underlying some anginal attacks, namely the vasoconstriction of large coronary vessels at the level of atherosclerotic plaques and the reflex vasoconstriction of small coronary arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1989

Preoperative identification of patients likely to have left ventricular dysfunction after aortic valve replacement. Participants in the Veterans Administration Cooperative Study on Valvular Heart Disease.

The purpose of this study was to identify preoperative and intraoperative variables predictive of left ventricular dysfunction 6 months after aortic valve replacement. Patients were considered to have postoperative left ventricular dysfunction if the end-diastolic-volume index was greater than or equal to 101 ml/m2 or if the ejection fraction was less than or equal to 0.50. Data from 180 patients entered into the Veterans Administration Cooperative Study on Valvular Heart Disease who had technically satisfactory cardiac catheterizations 6 months postoperatively were analyzed by a series of univariate and multivariate analyses. For the 88 patients with preoperative aortic stenosis, the most powerful predictor of postoperative left ventricular dysfunction in the final multivariate model was preoperative left ventricular ejection fraction (p = 0.0001), followed by preoperative myocardial infarction (p = 0.012), aortic valve gradient (p = 0.020), and incomplete coronary revascularization (p = 0.059). Abnormal preoperative left ventricular ejection fraction had a sensitivity of 72% and a specificity of 82% in identifying patients with postoperative left ventricular dysfunction. Preoperative left ventricular systolic-volume index greater than or equal to 40 ml/m2 had a similar sensitivity and specificity (79% and 84%, respectively). For the 36 patients with aortic regurgitation, preoperative left ventricular ejection fraction was again the most powerful predictor of postoperative left ventricular dysfunction (p = 0.013), followed by left ventricular systolic pressure (p = 0.038) and arteriovenous oxygen difference (p = 0.054). For the 56 patients with mixed aortic stenosis and regurgitation, left ventricular systolic pressure (p = 0.007) and preoperative myocardial infarction (p = 0.022) were the variables predictive of postoperative left ventricular dysfunction. Although many patients with preoperative left ventricular dysfunction experience improved left ventricular performance after aortic valve replacement, performance does not always return to normal. For patients with either aortic stenosis or regurgitation, the strongest predictor of postoperative left ventricular dysfunction is preoperative dysfunction. These data support the concept that patients with moderate or severe aortic stenosis or regurgitation should be operated on before the onset of significant left ventricular dysfunction.

Aortic Valve↗
PubMed1992

Recruitment strategies in the studies of left ventricular dysfunction (SOLVD): strategies for screening and enrollment in two concurrent but separate trials. The SOLVD Investigators.

SOLVD was a double-masked, placebo-controlled trial whose initial sample size goal was to randomize 6100 participants into two concurrent trials: treatment and prevention. The objective was to determine if participants with severe left ventricular dysfunction (left ventricular ejection fraction < or = 35%, with congestive heart failure (2569) and participants without overt heart failure (4228) had improved survival with angiotensin-converting enzyme inhibitors. Participants were identified from cardiac catheterization, echocardiography and radionuclide laboratories, and inpatient units. The treatment trial recruitment goal was attained 13 months ahead of schedule while recruitment for the prevention trial was extended 11 months beyond the scheduled time. Recruitment of relatively asymptomatic participants with a low ejection fraction in a hospital-based trial necessitated novel strategies. Coronary care units and clinics for follow-up of acute cardiac conditions, not typically employed in studies of chronic diseases, were useful recruitment sources. Different approaches to encourage participation also needed to be employed. Expanding selected entry criteria was evaluated and the success of varying strategies was reviewed. The authors recommend tailoring of strategies to the target population, staffing flexibility, principal investigator involvement, and broad entry criteria in recruitment activities.

Cardiac Output↗
PubMed1994

Neurohormones in patients with ischemic left ventricular dysfunction.

Measurements of plasma neurohormones in patients with left ventricular dysfunction are generally performed for research purpose rather than for diagnostic purpose or to guide therapy. These studies have shown that in patients with left ventricular dysfunction, several neurohormonal systems were activated, even in the absence of symptoms of congestive heart failure. This suggested that the cardiovascular system was not in a steady state and pointed out potential culprits for the progression of the disease. It has also been shown that the levels of several of these markers, particularly plasma norepinephrine, had an important prognostic value. Another value of neurohormonal studies obviously is the design of new therapeutic approaches aimed at improving symptoms and prognosis. In this respect, important therapeutic successes have been obtained with agents that interfere with the actions of some of these neurohormonal systems, such as with the use of the angiotensin-converting enzyme (ACE) inhibitors, particularly captopril and enalapril, and to a lesser extent, with beta-blockers. It can therefore be expected that, in the future, most patients with severe ischemic dysfunction will be treated with an ACE inhibitor. Nonetheless, neurohormonal control is not complete with these drugs; powerful vasoconstrictor forces, such as endothelin-1, remain activated, and an escape of angiotensin II from the control of ACE inhibition may exist. Thus, morbidity (e.g., progression towards congestive heart failure and angina pectoris) and mortality remain high despite treatment with ACE inhibitors. In the search for future improvements, the new generation of long-acting dihydropyridines is worth considering. Their afterload reducing action, coupled with powerful coronary vasodilation, might hypothetically delay the progression of ischemic LV dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Long-term outcome of left ventricular dysfunction after surgery for severe aortic stenosis.

Thirteen patients with severe aortic stenosis and left ventricular dysfunction (ejection fraction < 0.50, Group A) received echocardiographic evaluation before, and early and late after isolated aortic valve replacement. The results were compared with those of 11 aortic stenosis patients without left ventricular dysfunction (Group B). Using two-dimensional echocardiography, left ventricular diastolic internal diameter (LVIDd), left ventricular systolic internal diameter (LVIDs), left ventricular wall thickness (interventricular septum + posterior wall: LVWT), left ventricular fractional shortening (FS), left ventricular mass index (LVMI) and left ventricular end-systolic wall stress (ESWS) were assessed before (Pre), at one month (Early) and 4-7.6 (mean 5.5 +/- 1.0) years (Late) after operation. In the early postoperative period in Group A, significant decrease was observed in LVIDd (5.4 +/- 0.8 to 4.5 +/- 1.0 cm, p = 0.010), LVWT (3.3 +/- 0.7 to 2.9 +/- 0.7 cm, p = 0.027) and LVMI (336 +/- 149 to 222 +/- 112 g/M2, p = 0.013). From the early to late postoperative period FS showed significant improvement in both groups (0.23 +/- 0.12 to 0.32 +/- 0.12 in Group A, p = 0.025 and 0.27 +/- 0.07 to 0.36 +/- 0.07, p = 0.014). However, changes of other parameters were not significant and LVMI in Group A remained twice as high as the normal value. It is concluded from the above results, that LV contraction in aortic stenosis patients with preoperative left ventricular dysfunction improved during the late postoperative period. Although LVMI in the early postoperative period significantly decreased as compared with the preoperative value, it showed no further improvement and remained at an abnormally high level. Therefore, early surgical treatment of severe aortic stenosis before appearance of LV dysfunction should be recommended for postoperative recovery from LV hypertrophy.

Aged↗
PubMedDate not supplied

Pulmonary venous flow in cardiac tamponade: influence of left ventricular dysfunction and the relation to pulsus paradoxus.

The pattern of left atrial filling was studied in nine closed-chest dogs during cardiac tamponade before and after production of microembolic left ventricular dysfunction produced by intracoronary injection of 54 +/- 4 microns (SD) microspheres. With cardiac tamponade, a significant increase in the ratio of systolic/diastolic pulmonary venous flow velocity integral both before (1.65 +/- 0.24 versus 2.77 +/- 0.43 [SE], p less than 0.05) and after production of left ventricular dysfunction (0.57 +/- 0.12 versus 1.77 +/- 0.44, p less than 0.05) was seen. Compared with baseline, cardiac tamponade caused a significant inspiratory decrease in systolic pulmonary venous velocity both before (7.3 +/- 2.0 versus 1.2 +/- 1.4 cm/sec) and after left ventricular dysfunction (3.4 +/- 0.4 versus 1.0 +/- 0.9 cm/sec, both p less than 0.05). The magnitude of respiratory variation (expiration-inspiration) of the pulmonary venous flow velocity integral with tamponade was significantly greater before than after left ventricular dysfunction (1.6 +/- 0.2 cm versus 0.8 +/- 0.2 cm, p less than 0.05). A significant correlation was found between the inspiratory fall in aortic systolic pressure and the flow velocity integral of pulmonary venous flow before left ventricular dysfunction (r = 0.58, p less than 0.05). After coronary embolization, neither pulsus paradoxus nor significant respiratory variation (expiration-inspiration) of the pulmonary venous flow integral was observed with cardiac tamponade. In this model of cardiac tamponade and left ventricular dysfunction, left atrial filling occurs predominantly during ventricular systole. These changes may be helpful in recognizing hemodynamically significant pericardial effusion and have implications for the pathophysiology of cardiac tamponade.

Animals↗
PubMed1995

Reversible left ventricular dysfunction associated with Guillain-Barré syndrome--an expression of catecholamine cardiotoxicity?

The patient was a 76-year-old female who had a history of Guillain-Barré syndrome 3 years previously; ST-segment elevation was noted in association with reversible left ventricular dysfunction. Left ventrioculogram and coronary angiograms were normal and ergonovine test was negative during the chronic period of Guillain-Barré syndrome. She was hospitalized again due to the recurrence of Guillain-Barré syndrome. Two days later, ST-segment elevation in leads V2 through V5 prompted us to perform cardiac catheterization, although she did not complain of any chest symptoms. A large akinetic area was found mainly around the apex on left ventriculography, despite the lack of coronary stenoses. Peak creatine kinase and C-reactive protein were 400 IU/ml and 3.5 mg/dl, respectively. Left ventricular dysfunction was normalized within one week. During the acute phase of the cardiac episode, plasma norepinephrine and epinephrine were 1340 pg/ml and 112 pg/ml, respectively. I123 metaiodobenzyl-guanidine myocardial scintigram 3 weeks after the episode showed an extensive apical defect which was improved markedly 3 months later. We think that this reversible left ventricular dysfunction was due to the synergistic toxic effect of mildly increased catecholamine and transiently damaged sympathetic nerve endings in the myocardium, presumably due to Guillain-Barré syndrome.

3-Iodobenzylguanidine↗
PubMed1980

Exercise capacity in patients with severe left ventricular dysfunction.

Normal or near-normal exercise capacity has been thought to reflect normal left ventricular function. Many compensatory mechanisms could preserve exercise capacity in patients with severe left ventricular dysfunction. We evaluated exercise capacity using a treadmill exercise test in 26 patients with severe left ventricular dysfunction defined by a left ventricular ejection fraction of 30% or less by isotope ventriculography. One half of the patients had normal exercise capacity and a normal cardiothoracic ratio on chest x-ray. This study indicates that traditional predictors of left ventricular function that have been widely used in clinical evaluation of the patients with cardiac disease (cardiothoracic ratio and exercise capacity) can be normal in a significant number of patients with severe left ventricular dysfunction. Thus, left ventricular function cannot be accurately estimated using these traditional predictors and should be assessed quantitatively. The isotope ventriculogram appears to be ideal for this purpose.

Adult↗
PubMed1997

How European cardiologists perceive the role of calcium antagonists in the treatment of heart failure and left ventricular dysfunction.

In a poll of European cardiologists, one of the most popular of the given definitions of heart failure centres on the abnormality of ventricular function. However, opinion remains divided on the necessity of a distinction between diastolic and systolic heart failure, as it does on the value and procedures of stress testing. The 'no-reflow' phenomenon continues to pose a challenge in conditions requiring myocardial reperfusion, and precise identification of some heart disorders apparently remains difficult in many cases. Drug treatment of conditions like left ventricular dysfunction of arterial hypertension is open to continuing discussion, but calcium antagonists seem assured of an important role.

Calcium Channel Blockers↗
PubMed1995

Dobutamine echocardiography and thallium-201 imaging predict functional improvement after revascularisation in severe ischaemic left ventricular dysfunction.

OBJECTIVES: To evaluate the concordance between thallium-201 uptake and echocardiographic wall thickening, which are both indicators of potentially reversible myocardial dysfunction, in patients with chronic ischaemic left ventricular failure and to assess their relative contribution to predicting improvement in regional function after revascularisation in a subgroup. PATIENTS AND METHODS: 45 patients with chronic ischaemic left ventricular dysfunction (mean (SD) ejection fraction 25 (8)%) underwent echocardiography before and after dobutamine infusion (10 micrograms/kg/min). Of these, 22 patients underwent rest echocardiography at a mean (SD) of 9 (1) weeks after revascularisation. 201Tl imaging was performed during dobutamine echocardiography and at rest, 1, and 4 h after treatment with sublingual glyceryl trinitrate on two separate days. Potentially reversible dysfunction was thought to be present when a myocardial segment contained a Tl score of > or = 3 (ascending score 1-4), or showed improved wall thickening of a dysynergic segment during dobutamine stimulation. RESULTS: Of the 201Tl protocols, the redistribution scan 1 h after treatment with glyceryl trinitrate best demonstrated myocardial viability. Concordance between 201Tl and dobutamine induced wall thickening was 82% (kappa = 0.59) for detecting potentially reversible myocardial dysfunction before revascularisation (n = 45). Regional function improved in 18 of 22 patients after revascularisation. There were 168 dysynergic segments before intervention. The sensitivity of echocardiography and 201Tl imaging for detecting "recoverable" or viable segments after revascularisation was 87% and 92% respectively and specificity was 82% and 78% respectively (P = NS). CONCLUSIONS: Dobutamine echocardiography and 201Tl imaging may be used to predict mechanical improvement in dysynergic segments after revascularisation in patients with chronic ischaemic left ventricular dysfunction.

Adult↗
PubMed1989

Valvular surgery in the elderly.

In previous studies from this university, advanced age was identified as an independent predictor of operative mortality for valvular surgery. Therefore, between January 1982 and December 1986, early results were compared in 469 patients greater than 70 years old (Old; 74.0 +/- 3.4 years, mean +/- SD) and in 2,040 patients less than 70 years old (Young; 53.7 +/- 12.1 years). Patients underwent single- or multiple-valve repair or replacement with or without concomitant coronary artery bypass surgery. Data consisting of 31 clinical and angiographic variables were collected prospectively and were analyzed by univariate and multivariate statistics. Old patients were characterized by having more frequent left ventricular dysfunction (left ventricular ejection fraction less than 40%: Old, 33.5%; Young, 22.4%; p less than 0.001), coronary artery disease (Old, 54.5%; Young, 24.2%; p less than 0.001), and urgent surgery (Old, 15.6%; Young, 11.8%; p = 0.02). Aortic valve procedures (Old, 59.7%; Young, 40.1%; p less than 0.001) and concomitant coronary artery bypass surgery (Old, 46.4%; Young, 20.3%; p less than 0.001) were performed more commonly in the Old patient. Operative mortality occurred in 10.0% of Old patients compared with 5.6% of Young patients (p less than 0.001), and major morbidity (low-output syndrome, perioperative myocardial infarction, intra-aortic balloon pump counterpulsation, and stroke) occurred significantly more frequently (p less than 0.001) in the Old. Stepwise logistic regression identified that urgent operation (p = 0.002), mitral or double-valve surgery (p = 0.004), coronary artery disease especially when not treated by bypass surgery (p = 0.02), female gender (p = 0.02), and left ventricular dysfunction (p = 0.05) independently predicted operative death in the Old population. The significant predictors of mortality in the Young patient were urgent operation (p less than 0.001), New York Heart Association class IV (p less than 0.001), associated tricuspid valve disease (p = 0.002), decreased left ventricular function (p = 0.01), valvular re-replacement (p = 0.02), and increasing age (p = 0.03). The predicted probability of operative mortality in Old patients ranged between 0.9 +/- 0.5% and 76 +/- 16%. Elderly patients in good risk categories should be offered surgical intervention for correction of valvular lesions. Alternative therapy may be indicated in patients with multiple risk factors.

Age Factors↗
PubMed1993

Role of behavioral and psychological factors in mental stress-induced silent left ventricular dysfunction in coronary artery disease.

OBJECTIVES: We examined the relationship of the psychological profile to left ventricular dysfunction induced during mental stress. BACKGROUND: The contribution of psychological factors to mental stress-provoked silent myocardial ischemia has not been explored. METHODS: Thirty patients with chronic stable coronary artery disease and a reversible defect on stress thallium-201 imaging completed a psychological assessment by questionnaire and Structured Interview, serially administered mental stress and brief walking exercise. Blood pressure, electrocardiogram (ECG) and left ventricular indexes were obtained by ambulatory serial radionuclide ventriculography. Silent ventricular dysfunction was defined by a decrease > or = 0.05 in ejection fraction or > or = 1 mm in ST segment on the ECG in the absence of symptoms. RESULTS: Of the 30 patients, 15 (Group I) had evidence of silent left ventricular dysfunction during mental arithmetic. The other 15 (Group II) showed no change. In addition, 18 of 30 patients had this dysfunction during the Structured Interview. Both ischemic and nonischemic groups developed comparable and significant increases in heart rate and blood pressure. Group I patients were distinguished by higher scores on measures of aggressive responding (p < 0.001), trait anger (p < 0.0001), hostile affect (p < 0.003) and an index of behavioral reactivity (p < 0.003) and a lower score on anger control (p < 0.001). No other variables, including historical and clinical indexes, discriminated between the two groups. CONCLUSIONS: Patients with coronary artery disease and mental stress-provoked silent ventricular dysfunction were distinguished by a psychological profile consistent with emotional reactivity to social interaction and mental provocation, with anger as the predominant affective state. Patients with such a profile may be at risk of frequent silent left ventricular dysfunction.

Adult↗