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Persistent impairment of regional contraction of the left ventricle after restoration of blood flow following transient coronary occlusion has been termed "stunning," and reversible regional dysfunction has also been observed during recovery from exercise-induced regional ischemia. To determine whether limitation of subendocardial blood flow after exercise is a determinant of such dysfunction in the presence of chronic coronary stenosis, nine conscious chronically instrumented dogs having an Ameroid constrictor were studied before, during, and after treadmill runs that induced regional ischemia. During exercise, systolic wall thickening (%WTh, sonomicrometers) in the ischemic region decreased from a normal level of 22.1 +/- 9.1% at rest to 8.8 +/- 5.2% (+/- SD, P less than 0.01), whereas subendocardial blood flow (microspheres) in the ischemic region decreased from 0.75 +/- 0.25 to 0.45 +/- 0.27 ml.min-1.g-1 (P less than 0.05). %WTh in the ischemic region gradually improved after exercise but remained depressed (75% of control) at 30 min after the run (P less than 0.05). Postexercise dysfunction was not related to simultaneous regional hypoperfusion, since at 5 and 10 min after running there was a tendency toward subendocardial hyperemia (control 0.75 vs. 1.33 and 1.30 ml.min-1.g-1, NS) with a return to control by 30 min. Thus persistent regional dysfunction after exercise-induced regional ischemia in the conscious dog is not due to sustained subendocardial ischemia in the presence of chronic coronary stenosis and represents an example of myocardial stunning.

The view based on epidemiological and laboratory data that blood group A subjects (=A) have clinically significant higher thrombotic potential than blood group 0 subjects (=O), is supported by the present finding of a significantly higher platelet retention in A than 0. The completely normal AB0 distribution found among 71 cases of proven latent CHD, and the disproportionate excess of 0 vs. A in a consecutive series of 191 coronary artery bypass candidates apparently conflict with epidemiological data indicating a higher risk of achieving CHD in A than 0. The conflict may be solved by suggesting a) that the "thrombotic proneness" in A compared with 0 causes a poorer prognosis in CHD among the former, leaving a disproportionate excess of 0 among longterm CHD survivors, and b) that AB0-related factors have had an insignificant, independent impact on the evolution of preclinical coronary artery disease in our 71 men with latent CHD.

The function of blood platelets sampled from the coronary sinus and the superior vena cava was studied in 50 men with coronary artery disease at rest and during pacing-induced angina. At rest, a lower platelet aggregation and retention response was found in coronary sinus compared with vena caval blood. This may be due to refractoriness after previous platelet stimulation or to release of platelet inhibitors in the coronary circulation. During pacing-induced angina, lactate levels indicated that blood was sampled from ischemic myocardium in only 27 of the patients. Pacing-induced angina influenced platelet function differently in blood from ischemic and nonischemic regions. Adenosine diphosphate- and collagen-induced aggregation, platelet retention and plasma beta-thromboglobulin levels remained unchanged in blood from ischemic myocardium during pacing, but increased in blood from nonischemic regions. Thus, factors other than ischemia activated platelets in the coronary circulation during tachycardia-induced stress.

A positive exercise ECG test in a middle-aged man without confounding disease is a strong indicator of occult coronary heart disease. In the years following a positive test mortality, but CHD events vary considerably compared with subjects having normal exercise tests. If a second exercise test is positive in the same subjects years later, this signifies a disease which is prone to progress in a very severe way in the ensuing years. A first normal test followed by a second pathologic test has an intermediate prognostic significance compared with two normal tests years apart. The clinical course indicates that preventive measures should be taken after observing a positive exercise test, and even more importantly if two positive tests are observed years apart.

Myocardial scintigraphy with thallium-201 and electrocardiogram-gated left ventriculography with technetium-99m labelled red blood cells were applied in four groups of subjects: 25 with no signs or symptoms of cardiovascular disease (group 1), 28 with a "false" positive exercise electrocardiogram (group 2), 14 with angina pectoris and normal coronary angiograms (group 3), and 43 with angina pectoris and fixed coronary artery stenoses (group 4). In groups 1 and 4 the radionuclide findings were in accordance with clinical and invasive measurements. In groups 2 and 3 the most important finding was the lack of increase in left ventricular ejection fraction during exercise in about half of these subjects (even a decrease in 25%), indicating subnormal myocardial reserve. The additional finding of pathological myocardial biopsies in four of these patients suggests that asymptomatic ST depression in patients with normal coronary angiograms may in some cases represent an early, preclinical sign of cardiomyopathy.

Platelet function was studied in blood sampled from the caval vein of 56 patients through various heart catheters. Reduced platelet retention was the most consistent finding while aggregation was not influenced by the sampling procedure. Polyurethane (Cordis and Positrol) catheters affected platelets less than catheters of woven dacron (Sones and Zucker). Sones catheters increased plasma beta-thromboglobulin levels slightly, and some platelets were trapped in the Zucker catheters. Much the same reduction in retention was induced by heparinized as by other catheters. Platelet retention values had a poorer reproducibility than the other platelet function parameters in samples collected at intervals of 45 min, while an acceptable correlation existed between parallel samples. The influence on platelets of blood sampled via polyurethane catheters was very moderate, and should allow the detection of alterations in platelet functions that occur in the circulation.

Blood sampled from the coronary sinus was compared with blood collected simultaneously from the superior caval vein in 50 men with angiographically proven coronary heart disease. Primary, ADP-induced aggregation in coronary sinus blood was reduced by 14 per cent, collagen-induced aggregation by 10 and platelet retention by 16 to 30 per cent as compared with blood from the caval vein. The plasma levels of beta-thromboglobulin, platelet counts and number of circulating platelet aggregates were similar in parallel samples. The reduced platelet function in coronary sinus blood hardly reflects refractoriness after previous platelet stimulation, since no release or irreversible aggregation was induced. A reduced function might be the effect of direct depression induced in the coronary circulation. Most surprisingly, a selective thromboxane synthetase inhibitor (Dazoxiben) and acetylsalicylic acid normalized platelet aggregation but did not affect the low platelet retention response in coronary sinus blood. Thus, the reduced platelet function in coronary sinus blood is not only mediated via prostaglandins.

The parmacokinetics of disopyramide (DP) in 10 patients with imminent to moderate cardiac failure has been studied and compared with the results in normal volunteers. The biological half life of rapid distribution (T1/2 alpha) and of elimination (T1/2 beta) were increased (11.1 +/- 4.4 min and 9.7 +/- 4.2 h, respectively). Total body clearance (Clt) was decreased (0.467 +/- 0.215 ml . min-1 . kg-1), and the volume of distribution (Vd) was slightly reduced (0.610 +/- 0.1361 . kg-1), probably due to the lower cardiac index. After oral administration, the time of peak serum concentration was increased (139 +/- 89 min), and the mean peak serum concentration (2.4 +/- 0.8% dose . 1-1) was also higher than reported in normal subjects. Comparison of the areas under the concentration versus time curves after intravenous and oral administration (AUC i. v. and AUC oral) showed that DP was almost completely absorbed, its bioavailability being 97.5 +/- 15.0%.

The effect of timolol on blood platelet function was studied in coronary sinus and caval vein blood at rest and during pacing-induced angina in 20 patients with coronary heart disease. During pacing-induced angina, lactate measurements confirmed that coronary sinus blood was sampled from ischemic regions in 13 men. The ischemia did not influence platelet function. In blood from non-ischemic myocardium, platelet activation was found during pacing: the ADP-induced aggregation, platelet retention and plasma beta-thromboglobulin levels increased moderately but significantly. Timolol administration prevented this platelet activation, possibly by inhibiting catecholamine release from the myocardium, and reduced the ischemic response during pacing as judged from lactate measurements and ST depressions. It is concluded that timolol reduced platelet activation induced in non-ischemic regions of the heart during tachycardia stress as well as myocardial ischemia.

Determination of the effect of inotropic stimulation on regionally ischemic and hypokinetic myocardium is complicated when intravenous administration of the inotropic agent also causes stimulation of nonischemic adjacent and distant regions, thereby altering global ventricular hemodynamics. To obviate such events, 16 anesthetized swine were studied during regional inotropic stimulation by infusion of dobutamine hydrochloride (2.5 +/- 1 microgram/min) into the cannulated left anterior descending coronary artery. Coronary inflow was controlled by a pump in an extracorporeal circuit. Two groups of swine with different degrees of ischemia were studied. In the first group of animals (n = 8), reduction in coronary inflow to produce a fall in coronary artery pressure (CAP) from 114 +/- 7 mm Hg to 62 +/- 2 mm Hg caused a decrease in percent systolic wall thickening (%WTh) from 34.6 +/- 8.1% to 25.4 +/- 5.8% (p less than 0.005). In the second group of animals (n = 8), CAP was decreased to 46 +/- 5 mm Hg (control: 115 +/- 8 mm Hg) and % WTh decreased from 34.1 +/- 16.4% to 10.4 +/- 6.9% (p less than 0.001). Subendocardial blood flow was reduced from 1.41 +/- 0.38 ml/min/g to 0.65 +/- 0.13 ml/min/g (group 1, p less than 0.001) and from 1.08 +/- 0.22 ml/min/g to 0.24 +/- 0.08 ml/min/g (group 2, p less than 0.001). Regional infusion of dobutamine caused asynchronous ventricular contraction with early systolic augmentation in wall thickening followed by late systolic thinning. Therefore, during hypoperfusion regional myocardial function assessed by %WTh remained unchanged (26.2 +/- 5.8%, p = NS) in group 1 and decreased significantly to 1.6 +/- 5.1% (p less than 0.041) in group 2. Subendocardial blood flow decreased to 0.44 +/- 0.15 ml/min/g in group 1 (p less than 0.005) and to 0.15 +/- 0.07 ml/min/g in group 2 (p less than 0.012). To account for the augmented early systolic thickening that occurred during asynchronous contraction, a myocardial work index was developed in which the sum of the instantaneous left ventricular pressure-wall thickness product was calculated for estimation of regional myocardial work. Increases in this work index were apparent with the addition of dobutamine at both levels of hypoperfusion. This significant enhancement in regional myocardial function in group 2 caused a significant increase of 16% (p less than 0.009) in overall left ventricular power during ejection. Thus, regional inotropic stimulation with dobutamine caused enhancement of maximum work of the ischemic myocardium in the steady state despite a further decrease in subendocardial blood flow.

Coronary heart disease (CHD), previously neither diagnosed nor suspected, was strongly suspected in 115 of 2014 men aged 40-59 years during a cardiovascular survey examination. Sixty-nine of 105 men who underwent diagnostic coronary angiography had pathologic angiograms. Twenty-six of these 69 had angina pectoris (AP) with and without pathologic exercise ECGs and 43 had pathologic exercise ECG as the only indicator of CHD. The extent of coronary artery changes was similar in the two groups. The men without AP were in almost all respects similar to 1832 men labelled as normals. The men with AP differed in several respects from their non-AP angiographic counterparts and from their non-AP angiographic counterparts and from the normals: they had more dyspepsia, a higher stress score, higher serum cholesterol and triglycerides, lower antithrombin III levels in the blood and lower blood platelet retention values. These results indicate that coronary artery disease with and without AP may represent somewhat different pathogenetic entities.

A young man with a fistula between the right femoral artery and vein due to bullet wound presented 6 years later with exertional dyspnea and palpitations and venous insufficency of the right leg. Angiography showed a wide (greater than 20 mm) arteriovenous fistula. Moderate cardiac hypertrophy and cardiac output 14.8 l/min were found. During division and closure of the fistula, 8 l/min flow was measured in the right external iliac artery. The cardiac symptoms disappeared immediately and the venous insufficiency gradually.

Myocardial ischemia without symptoms (= silent ischemia = Sl) has become a well known clinical entity in subjects with heart disease and in apparently healthy subjects. Detection of Sl is easiest and least expensively done with exercise ECG-testing (X-ECG). Data on the significance of Sl in the present report is derived from long-term follow-up of 2014 men aged 40-59 yrs, studied 1972-75, restudied in 1979-81 and 1986-88. The sources of information are: 1) 50 men with Sl detected with X-ECG/coronary angiography in 1972-75; 2) subjects with positive X-ECG in 1979-81 (but not in 1972-75); 3) preliminary data from the last follow-up study; and 4) complete data on cardiovascular mortality by Aug. 1987. The survey data indicate: a) Sl detected with X-ECG, confirmed with angiography is an indicator of later severe CHD-complications over 12-15 yrs; b) positive X-ECGs (not validated invasively) increase the risk of future CHD events and death from CHD 2-4 fold compared with subjects with normal X-ECG of similar age; c) limited isotope studies from the 1986-88 study indicate a very high specificity of a positive X-ECG in CHD, and d) cardiovascular mortality is very accurately predicted by factors known to be associated with the development of CHD. In accordance with the world literature, Sl is frequently observed in apparently healthy middle-aged and old men, and increases the risk of future CHD considerably when encountered.

Sixty-six consecutive patients less than 40 years of age with angiographically documented coronary artery disease and coronary heart disease took part in a study aimed at (1) identifying the presence of factors which might explain the premature onset of ischaemic heart disease, and (2) assessing the distribution and severity of the coronary artery lesions. For comparisons we have used a study of risk factors in 1832 men defined as "normals" according to a recent comprehensive examination. The findings show that the typical early onset coronary heart disease case is an overweight, heavily smoking male "blue collar" worker, with high serum levels, a marginally raised blood pressure, and a high prevalence of coronary heart disease among first degree relatives. Coronary angiography showed a preponderance of one vessel disease. In particular, left anterior descending artery lesions were common, which might have contributed to the early manifestation of disease.

A rare case of a rhabdomyoma originating from the surface of the right atrium in a 20-year-old female is reported. The tumor showed electrical activity and caused both outflow obstruction and tamponade symptoms. It was successfully removed by a right-sided thoracotomy. The clinical course, diagnostic investigations, and the therapeutical approach of this rare lesion are discussed.

Disopyramide exerts a quinidinelike effect on the heart and is a valuable drug for treating atrial and, especially, ventricular tachyarrhythmias. The therapeutic plasma concentration of disopyramide is thought to be 2.0-4.0 (5.0) microgram/ml. We here report the cardiac effects of a high dose of disopryamide in a patient with extensive coronary artery disease complicated by ventricular extrasystoles. At plasma levels above approximately 7.0 micrograms/ml, heart rate was decreased, while PQ interval, width, and QT interval were increased. At concentrations above approximately 6.0 micrograms/ml, disopyramide exerted negative intropic effects as judged by increases in mean right atrial, pulmonary arteriolar, and pulmonary capillary venous pressures and a decrease in cardiac output.