Epicardial fat, rather than pericardial fat, is independently associated with diastolic filling in subjects without apparent heart disease.

BACKGROUND AND AIM: Epicardial and pericardial fat are separate fat depots surrounding the heart. Previous studies found epicardial fat to be associated with diastolic dysfunction, but they had some limitations. Pericardial fat association with diastolic dysfunction was not examined. Our aim was to assess the relation of epicardial and pericardial fat with diastolic filling. METHODS AND RESULTS: In 73 volunteers without known heart disease or complaints, using echocardiography, we measured epicardial and pericardial fat thickness from long(LAX) and short(SAX) axis views and assessed diastolic filling: mitral inflow (E/A ratio, E wave deceleration time[DT]), pulmonary vein flow (systolic/diastolic ratio [S/D], systolic filling fraction[SFR], late retrograde velocity[Ar]), color M-mode flow propagation velocity [Vp], and tissue Doppler derived mitral early annular velocities at the septum [e' sep] and lateral wall [e'-lat]. By Spearman's correlation, epicardial fat from LAX had a weak, but statistically significant correlations with several diastolic filling indices (SFR{rs = 0.29, P = 0.02}, Ar{rs = 0.3, P = 0.01}, Vp{rs = -0.3, P = 0.01}, e' sep{rs = -0.23, P = 0.04}, e' lat{rs = -0.26, P = 0.03}). In multivariate logistic regression model adjusting for age, gender, diabetes, systolic blood pressure and left ventricle mass index, epicardial fat thickness from LAX (and not from SAX) was the only independent predictor of e' [e' sep < 8: OR = 1.8, 95%CI = 1.1-2.9; e' lat<10: OR = 1.6, 95%CI = 1.01-2.6]. After adjustment, Pericardial fat measured from LAX was independent predictor of e' lat only[e' lat < 10:OR = 1.3, 95% CI 1.03-1.6). CONCLUSIONS: Epicardial fat measured from LAX is an independent predictor of myocardial relaxation. Pericardial fat independent association with diastolic filling is uncertain.

Mechanisms linking nonalcoholic fatty liver disease with coronary artery disease.

The most common cause of death in patients with nonalcoholic fatty liver disease (NAFLD) is coronary artery disease (CAD), not chronic liver disease. Fatty liver increases cardiovascular risk by classical (dyslipidemia, hypertension, diabetes) and by less conventional mechanisms. Common pathways involved in the pathogenesis of fatty liver and CAD includes hepatic insulin resistance and sub clinical inflammation. The hepatic insulin resistance state of fatty liver infiltration is characterized by increased FFA, which causes lipotoxicity and impairs endothelium-dependent vasodilatation, increases oxidative stress, and has a cardio toxic effect. Additional metabolic risk factors include leptin, adiponectin, pro inflammatory cytokines [such as IL-6, C-reactive protein and plasminogen activator inhibitor-1 (PAI-1)], which together lead to increased oxidative stress and endothelial dysfunction, finally promoting coronary artery disease (CAD). When classical risk factors are superimposed on fatty liver accumulation, they may further increase the new metabolic risk factors, exacerbating CAD. The clinical implication is that patients with NAFLD are at higher risk (steatohepatitis, diabetes, obesity, atherogenic dyslipidemia) and should undergo periodic cardiovascular risk assessment including the Framingham score, cardiac effort test, and measurement of intimae-media thickening of the carotids arteries. This may improve risk stratification for CAD.

Effect of mibefradil, a T-type calcium channel blocker, on morbidity and mortality in moderate to severe congestive heart failure: the MACH-1 study. Mortality Assessment in Congestive Heart Failure Trial.

BACKGROUND: Calcium antagonists have proved disappointing in long-term congestive heart failure (CHF) studies. Mibefradil, a new calcium antagonist that selectively blocks T-type calcium channels, has been shown to be an effective antihypertensive, antianginal, and anti-ischemic agent, and because of its different mechanism of action, it may be beneficial as adjunct therapy in CHF patients. METHODS AND RESULTS: This multicenter, randomized, double-blind study compared mibefradil with placebo as adjunct to usual therapy in 2590 CHF patients (NYHA class II to IV; left ventricular fraction <35%). The initial 50-mg daily dose of mibefradil was uptitrated to 100 mg after 1 month and continued up to 3 years. Patients were monitored at 1 week; 1, 2, and 3 months; and every 3 months thereafter. All-cause mortality, cardiovascular mortality, and cardiovascular morbidity/mortality were analyzed by use of the log-rank test (alpha=0.05). Substudies included exercise tolerance, plasma hormone and cytokines, echocardiography, and quality of life. Total mortality was similar between mibefradil- and placebo-treated patients (P=0.151). The 14% increased risk of mortality with mibefradil in the first 3 months was not statistically significant (P=0.093). Treatment groups had similar cardiovascular mortality (P=0.246), cardiovascular morbidity/mortality (P=0.783), and reasons for death or hospitalization. Patients comedicated with mibefradil and antiarrhythmics (class I or III), including amiodarone, had a significantly increased risk of death. Substudies demonstrated no significant differences between treatments. CONCLUSIONS: When used as adjunct therapy, mibefradil did not affect the usual outcome of CHF. The potential interaction with antiarrhythmic drugs, especially amiodarone, and drugs associated with torsade de pointes may have contributed to poor outcomes early in the study.

Prognostic value of noninvasively obtained left ventricular contractile reserve in patients with severe heart failure.

OBJECTIVES: The present study sought to evaluate the prognostic value of contractile reserve measured noninvasively during dobutamine infusion in patients with severe heart failure. BACKGROUND: In patients with severe heart failure there is a great need for objective criteria to define candidates for heart transplantation or intensive medical treatment. Cardiac pumping performance reserve has been shown to have excellent prognostic value in patients with cardiogenic shock. METHODS: Cardiac peak power, an afterload-independent contractility index, was measured noninvasively at rest and at peak dobutamine inotropic stimulation. Contractile reserve was defined as the difference between maximal cardiac power at peak dobutamine dose and baseline value. Maximal cardiac power was calculated from the maximal product of validated central arterial pressure and aortic flow. RESULTS: Results were obtained from 52 subjects (42 patients, 10 control subjects). Twenty-two patients were in New York Heart Association functional classes III and IV. Of nine patients with a contractile reserve < 1.5 W/ml, eight died during the 3-year follow-up period. In contrast, all survivors had a contractile reserve > 1.5 W/ml. Using multiple logistic regression analysis, contractile reserve was shown to be the only predictor of survival. CONCLUSIONS: Contractile reserve measured noninvasively during dobutamine infusion is a valuable prognostic indicator in patients with severe heart failure, with added value to ejection fraction.

The MB fraction of creatine phosphokinase. An indicator of myocardial involvement in acute pericarditis.

An elevated level of the MB fraction of creatine phosphokinase (CPK) with normal serum myoglobin and normal CPK values was found in a case of acute idiopathic pericarditis. The elevated serum CPK-MB isozyme is suggested to be an indicator of myocardial involvement accompanying acute pericarditis. The normal CPK and serum myoglobin values and the pattern of rapid decrease of CPK-MB level ruled out the possibility of acute myocardial infarction.

Treatment and outcome of patients with acute myocardial infarction and prior cerebrovascular events in the thrombolytic era: the Israeli Thrombolytic National Survey.

BACKGROUND: Patients with a history of stroke presenting with acute myocardial infarction (MI) are often excluded from thrombolytic therapy owing to fear of intracranial hemorrhage. Few data, however, are available on the risks vs the benefits of thrombolysis in patients with an acute MI and a prior cerebrovascular event (PCE). METHODS: Data were derived from 2 nationwide surveys of 2012 consecutive patients with acute MI admitted to all 25 coronary care units in Israel during 1992 and 1994. Thrombolytic therapy was given to patients with a PCE at the discretion of the treating physicians. Outcomes were compared between patients with an acute MI with and without a PCE and between patients with a PCE treated with or excluded from thrombolysis. RESULTS: Patients with a PCE (n = 115 [6%]) were older, with higher rates of atherosclerotic risk factors and in-hospital complications than their counterparts without a prior event (n = 1897). They were treated less often with thrombolysis or mechanical reperfusion. The 1-year mortality rates were higher among patients with a PCE (28% vs 19%, P<.01), but not after multivariate adjustments for clinical characteristics (adjusted hazard ratio, 1.08; 95% confidence interval, 0.75-1.55). Patients with an acute MI and a PCE who were treated with thrombolysis (n = 29 [25%]) were compared with 46 patients found ineligible for thrombolysis primarily because of their PCE. The timing of the PCE was comparable in both groups (one fifth in the preceding year), while prior transient ischemic attacks were more prevalent among patients who had undergone thrombolysis. The patients who were treated with thrombolysis (n = 29) were older, had a higher rate of anterior infarction, and, while in the hospital, received aspirin, anticoagulants, and beta-blockers more often than their counterparts (n= 46). In-hospital intracranial hemorrhage did not occur in either group. The 1-year mortality rates were 2-fold higher among patients who had not undergone thrombolysis compared with those who had (33% vs 18%; adjusted hazard ratio, 2.44; 95% confidence interval, 0.78-7.64). CONCLUSIONS: These findings, derived from 2 nationwide surveys of consecutive patients with acute MI, suggest that patients with PCEs have an adverse outcome attributed to their older age and less favorable risk profile. Thrombolytic therapy, however, based on our preliminary data, may be beneficial in selected patients with an acute MI with a nonrecent PCE.

Detection of chest pain of non-cardiac origin at the emergency room by a new non-invasive device avoiding unnecessary admission to hospital.

Recent advances in the treatment of acute coronary syndromes has raised awareness that prompt presentation for chest pain may be life saving. Most patients presenting with chest discomfort have a non-ischaemic ECG on presentation, but are routinely admitted to hospital because of diagnostic uncertainty for occult MI or ischaemia. We tested a new non-invasive device that measures central aortic pressure changes (dP/dtejc): an accepted index of myocardial performance that could be added to the diagnostic triage of ischaemia in the ER avoiding unnecessary admissions. We followed 85 patients presenting at the ER with acute chest pain. In 72 patients, negative ECG and myocardial enzyme dynamics ruled out coronary origin during the first 24 h after admission. In 8 of the 72 patients, coronary catheterisation found normal coronary arteries. In this group, average dP/dtejc was 163 (range 92-232). In 35 patients in whom the new non-invasive cardiac performance index dP/dtejc was above a threshold of >150, acute MI was ruled out. In 13 patients, acute chest pain had coronary origin confirmed by ECG and/or positive enzymes. The average dP/dtejc in this group was 117 (range 61-149). The dP/dtejc values were found to be significantly higher in patients without acute MI (p<0.001). Preliminary findings suggest that nearly 40% of patients presenting with acute chest pain could be spared the risks and costs of unnecessary hospital admission and more invasive cardiac testing by simply adding a easy to use, immediately obtained, test to the diagnostic protocol, and using a threshold of dP/dtejc>150 to rule out heart attack.

Validation of a method for noninvasive measurement of central arterial pressure.

The goal of this study was to validate a newly improved noninvasive method for calibrated measurement of the ascending portion of the central arterial pressure wave in humans. Noninvasive pressure waveforms were generated by measuring the time delay between the R wave of the electrocardiogram and onset of brachial artery flow (by Doppler) during computer-controlled upper arm cuff deflation. This delay shortens with falling cuff pressure (becoming near constant at and below diastolic pressure), so that a plot of pressure versus time delay yields the ascending portion of the arterial waveform. These waveforms were compared with simultaneous invasive ascending aortic pressures in 57 adult patients (31 by fluid manometer [group A] and 26 by catheter-tipped micromanometer [group B]) during routine cardiac catheterization. Patient age ranged from 26 to 77 years. Eighty percent of group A patients and 40% of group B had coronary artery disease. Noninvasive systolic and diastolic pressures were very similar to invasive values in both groups (Pni = 0.98 x Pi, r = 0.99, p < 0.0001). Instantaneous pressure differences between waveforms were also similar in both groups, averaging between 4.5 and 5.5 mm Hg. Micromanometer and noninvasive pressure data were also obtained before and after intravenous nitroglycerin (n = 5) and isometric handgrip (n = 8) and demonstrated good agreement. A potential application of these pressures is for estimating maximal ventricular power to assess systolic function. This was tested using invasive pressure-volume data from four patients under a variety of conditions (exercise, pacing, etc.).(ABSTRACT TRUNCATED AT 250 WORDS)

A single dose of cilazapril improves diastolic function in hypertensive patients.

We studied the effect of a single dose of cilazapril, 5.0 mg orally, on systolic and diastolic cardiac function in eight hypertensive patients using a double-blind crossover placebo-controlled design. All patients had concentric left ventricular hypertrophy (measured by echocardiography), unimpaired systolic function (measured by radionuclide ventriculography), and long-standing hypertension treated by a combination of beta-blockers and diuretics. Radionuclide scintigraphy was performed with cilazapril and placebo, given one week apart. A two-week washout period of all cardioactive drugs preceded the study. Within three hours after oral administration of cilazapril, the time to peak filling rate of the left ventricle, expressed as a percentage of diastole, was reduced from 44.5 +/- 13.2 percent to 31.2 +/- 7.2 percent (p less than 0.05). Systolic blood pressure was also significantly reduced by cilazapril. Heart rate was slightly reduced. Left ventricular ejection fraction, peak filling rate, and the absolute time to peak filling rate were not significantly altered. Cilazapril improves a sensitive index of diastolic cardiac function in hypertensive patients.

Left ventricular peak power during exercise: a noninvasive approach for assessment of contractile reserve.

Cardiac peak power, a contractility index based upon instantaneous changes in intracavitary pressure and systolic peak flow, was measured at rest and during supine exercise in 26 patients with coronary artery disease and 8 healthy subjects. The pathophysiological significance of this index was compared with left ventricular ejection fraction (LVEF) during exercise. Cardiac peak power, ejection fraction, end-diastolic volume, stroke volume, cardiac output and systemic vascular resistance were measured at rest, during three stages of supine bicycle ergometry and two stages of recovery. Cardiac peak power increased continuously in healthy subjects, from 5.4 +/- 0.8 W/ml at rest to 11.4 +/- 3.1 W/ml at peak exercise, p < 0.001. In patients, peak power increased initially, reached a plateau in stage 2, and subsequently remained unchanged in stage 3 (5.6 +/- 2 versus 5.6 +/- 1.6 W/ml, p = ns). Ejection fraction demonstrated a flat response during exercise in patients, contrasting with a 42% increase in cardiac peak power. The lack of increase in ejection fraction was attributed to its dependence on afterload. Peak power showed no correlation with systemic vascular resistance (r = 0.01, p = ns). In a subgroup of patients with low resting LVEF (LVEF = 26% +/- 7%), peak power increased 70% during exercise, from 2.0 +/- 0.7 to 3.5 +/- 1.7 W/ml, p < 0.05, in contrast to a flat ejection fraction response. Thus, cardiac peak power, a relatively afterload-independent index of left ventricular performance and contractility can be obtained noninvasively during exercise.

Radionuclide ventriculography and central aorta pressure change in noninvasive assessment of myocardial performance.

Systolic pressure-volume diagrams were obtained noninvasively by measuring the systolic central aortic pressure with a new device and by combining the pressure measurements, thus obtained, with absolute volume measurements obtained by radionuclide ventriculography during ejection. By dividing the peak power by the time elapsed from the beginning of ejection to the peak power point, the ejection rate of change of power (ERCP) was calculated. The ability of this index to assess left ventricular function at rest and exercise was evaluated in ten healthy subjects. ERCP proved to be more sensitive than global left ventricular ejection fraction increasing fivefold from rest to exercise compared with only 20% increase in global ejection fraction. ERCP increased dramatically postexercise from 3411 +/- 2173 to 18,162 +/- 14,633 gm/sec2, median 12,750, 95% confidence interval 9700-29,600, in healthy, while in patients it increased twofold from 2637 +/- 824 to 5062 +/- 1897 gm/sec2, median 4070, 95% confidence interval 2800-7030, p less than 0.001. ERCP had an excellent discriminative power in differentiating healthy subjects from patients, having 100% sensitivity, 90% specificity, 95% accuracy, 95% positive predictive value, and 90% negative predictive value. Thus, this noninvasive index seems to have a more comprehensive ability to evaluate changes in left ventricular function and shows a promising potential for clinical applications.

Comparative evaluation of a new formulation of isosorbide dinitrate oral spray and sublingual nitroglycerin tablets.

The magnitude and time course of the hemodynamic effect of a new formulation of an aqueous solution of isosorbide dinitrate (ISDN) spray were compared with those of sublingual nitroglycerin (NTG) tablets in 12 patients with chronic congestive heart failure. The patients received, in a random order, ISDN spray, 2.5 mg, or sublingual NTG, 0.8 mg. Hemodynamic measurements were performed before and at 1, 3, 5, 10, 20, 30 and 60 minutes after each drug. The second drug was given only after return of the hemodynamic parameters to baseline, plus a washout period of 2 hours. The hemodynamic variables measured were comparable at baseline. Both drugs produced hemodynamic improvement including a decrease in pulmonary capillary wedge pressure (PCWP), right atrial pressure and systemic and pulmonary vascular resistances. Only ISDN spray significantly increased cardiac output. The onset of action of ISDN spray was significantly more rapid than that of NTG. This was primarily evident in the decrease in PCWP. With ISDN spray the decrease started at 1 minute after administration, and at 3 minutes a decrease of 8.6 mm Hg was already found. The corresponding value for sublingual NTG was 1.6 mm Hg. The difference was highly significant (p less than 0.02). The peak effect of ISDN spray on PCWP and right atrial pressure was greater than that of NTG. Thus, the onset of the hemodynamic effect of the new formulation of ISDN spray is much more rapid than that of sublingual NTG tablets. At the doses used, the magnitude of the effect of the ISDN spray on some of the hemodynamic variables is greater than that of sublingual NTG.

Transdermal nitroglycerin patches for silent myocardial ischemia during antianginal treatment.

Because silent ischemia is not associated with an increase in heart rate and, being asymptomatic, its treatment requires constant therapeutic plasma levels of the drug used, a transdermal nitroglycerin patch (Deponit) was selected for treatment of this condition. Eight patients with documented silent ischemia were studied. All patients also had angina on effort treated with calcium antagonists (n = 8) and beta blockers (n = 6). They were evaluated by 24-hour ambulatory electrocardiographic monitoring. The transdermal nitroglycerin patch, 20 to 30 mg/24 hours, reduced the number of silent ischemic episodes from 9.25 +/- 5.52 to 2.4 +/- 2.0 episodes per 24 hours (p less than 0.001). The maximal ST-segment depression was reduced from 3.1 +/- 0.7 to 0.9 +/- 0.7 mm (p less than 0.001). Ventricular premature beats were significantly reduced, by 50%. Symptomatic ischemic episodes were completely suppressed. Thus, transdermal nitroglycerin, in moderate doses, is effective in suppressing silent ischemia in patients with angina pectoris who have silent ischemic episodes despite treatment with other antianginal agents.

Prevention of creatine kinase-MB release in coronary artery disease and pacing-induced myocardial ischemia by isosorbide dinitrate spray.

The effect of isosorbide dinitrate (ISDN) spray on release of the isoenzyme creatine kinase-MB (CK-MB) after myocardial ischemia induced by atrial pacing was evaluated in 8 patients with coronary artery disease. Atrial pacing to ischemia (ST-segment depression of greater than or equal to 1.5 mm for greater than or equal to 80 ms) resulted in elevation of CK-MB levels in plasma drawn from the coronary sinus, from 1.8 +/- 1.5 to 6.8 +/- 7.0 ng/ml (p less than 0.001) at 30 minutes after onset of ischemia. When atrial pacing was repeated at the same rate after 1 squirt of ISDN spray, 1.25 mg, the CK-MB levels were not altered despite significant ischemic ST-segment depression. It is concluded that ISDN prevents the process responsible for myocardial release of CK-MB, being either micronecroses or a reversible consequence of ischemia.

Effects of a single dose of isosorbide-5-mononitrate on the left ventricular diastolic function in systemic hypertension.

The effect of a single dose of isosorbide-5-mononitrate on left ventricular (LV) diastolic function was assessed by radionuclide ventriculography in 18 hypertensive patients. The effect of the mononitrate on atrial filling also was assessed. As expected, there was a significant decrease in mean blood pressure (120 +/- 17 to 102 +/- 18 mm Hg, p less than 0.005). Global LV ejection fraction did not show a significant change, increasing slightly from 64 +/- 9 to 68 +/- 8% (difference not significant). The mononitrate prolonged the time to peak filling rate from 176 +/- 36 to 195 +/- 29 ms (p less than 0.0001). The percentage of time to peak filling rate from diastole also increased, from 46 to 53% (p less than 0.05), whereas the normalized peak filling rate did not change (2.36 +/- 0.6 to 2.31 +/- 0.6 end-diastolic volumes/s, difference not significant). This effect on LV diastolic function was closely related to a certain reduction in preload, as suggested by the reduction in mean left atrial filling (45 +/- 12 to 40 +/- 13 counts/s, p less than 0.005) and LV diastolic counts, suggesting that the "impairment" of diastolic function induced by nitrates is secondary to the reduction in venous return to the left atrium. The mononitrate did not affect the mean right atrial filling rate (50 +/- 12 to 52 +/- 13 counts/s) and the right ventricular end-diastolic counts, suggesting a primary vasodilatory effect of nitrates on the pulmonary vascular bed.

Factors presaging early recurrent myocardial infarction ("extension").

A prospective study of 200 consecutive patients with acute myocardial infarction was undertaken to characterize the frequency and severity of early recurrent infarction (extension), manifested by secondary plasma MB creatine kinase (CK) and myoglobin peaks, and to identify patients at particularly high risk. Serial MB CK and myoglobin determinations and continuous electrocardiographic recordings were obtained in all patients for 14 days, and serial radioventriculograms were obtained in selected patients. Chest pain and S-T segment changes occurred often, in 57 and 43 percent, respectively, of the entire group of patients. However, a secondary rise in plasma MB CK levels indicative of recurrent infarction, occurring an average of 10 +/- 4 days after the initial infarct, was evident in only 17 percent of patients. Forty-three percent (25 of 58) of patients with initial subendocardial infarction exhibited recurrent infarction compared with only 8 percent of those with initial transmural infarction. The mortality rate was 7 percent in patients with subendocardial infarction without early recurrence compared with 16 percent among those with recurrent. Logistic regression analysis indicated that obese women with initial subendocardial infarction and repeated episodes of prolonged chest pain had a high probability rate (60 percent) of recurrence in contrast to the low probability (2 percent) in patients without these features. Thus, early recurrent infarction is frequent after subendocardial infarction and is associated with a marked increase in mortality. These results suggest that patients with subendocardial infarction are at particularly high risk for recurrent infarction and that patients with this type of infarction require vigorous monitoring and prolonged surveillance.

Increased exercise tolerance and reduced duration of ischemia after isosorbide dinitrate oral spray in angina pectoris.

The prophylactic and therapeutic anti-ischemic efficacy of isosorbide dinitrate (ISDN) oral spray was assessed in 10 patients with coronary artery disease and stable angina pectoris. The patients entered a randomized crossover study of ISDN spray and placebo, involving bicycle exercise testing. Each patient underwent 2 exercise tests at least 4 hours apart. Immediately before initiation of exercise they received either ISDN spray or placebo and crossed over during the other test. ISDN spray delayed the onset of anginal pain by about 40%, from a mean of 5.1 +/- 1.4 minutes with placebo to 7.2 +/- 1.3 minutes with the active drug (p less than 0.001). Time of onset of ST-segment depression was also significantly prolonged, from 7.1 +/- 1.5 minutes with placebo to 10.2 +/- 1.2 minutes with ISDN (p less than 0.001). The patients achieved a higher double product at onset of pain with ISDN than with placebo. The drug also reduced the time of disappearance of pain after discontinuation of exercise from 3.2 +/- 0.7 to 2.1 +/- 0.8 minutes (p less than 0.001), and the time of disappearance of electrocardiographic changes from 4.2 +/- 0.6 to 2.5 +/- 0.8 minutes (p less than 0.005). These findings indicate that oral ISDN spray is an effective prophylactic for exercise-induced angina. Its rapid onset of action makes it especially suitable for usage immediately before exercise.

Acute myocardial infarction complicating viper bite.

An acute myocardial infarction was induced by Vipera palaestinea venom in a young patient. The diagnosis was confirmed by cardiac catheterization, which showed a segmental contraction abnormality but normal coronary arteries.

Gorham's disease of the clavicle with bilateral pleural effusions.

A patient with Gorham's disease (massive osteolysis, disappearing bone disease) of the right clavicle had bilateral sanguinous pleural effusions. Complete cure was achieved by removal of the bony remnants with the hemangiomatous mass which caused bone destruction, and by obliteration of the pleural spaces using repeated talcum insertion. In six out of seven previously described cases of Gorham's disease with pleural effusions, the patients died, while the only survivor had a unilateral chylous effusion.

MB isoenzyme of creatine phosphokinase. Indicator of ischemia in coronary arterial disease.

After undergoing a stress test that showed abnormal findings, a patient with severe coronary arterial disease had an elevated concentration of the MB isoenzyme of creatine phosphokinase, in the presence of normal levels of creatine phosphokinase and myoglobin in the serum.