SUMMARY We studied 25 anesthetized and thoracotamized dogs before and during 5 hours of acute regional myocardial ischemia. Krypton-81m ( 8Xm Kr) was infused constantly into the aortic sinuses. The myocardial equilibrium of this tracer was used to image and assess the distribution of regional myocardial perfusion using a gamma camera and digital computer. The epicardial ECG was recorded, S-T segment elevation and the loss of R and appearance of Q waves were measured, and the plasma activity of creatine kinase (CK) was determined in aortic and coronary venous blood throughout these experiments. Ten dogs underwent left anterior descending coronary artery (LAD) narrowing for 5 hours and received no drugs. Five dogs received nifedipine 13 fig/kg, and another five received 1.0 /ig/kg intravenously 30 minutes after LAD narrowing. Those dogs receiving nifedipine, 13 fig/kg, showed a 30% fall in aortic pressure, a 12% rise in heart rate, and an extension of regional ischemia. The ECG showed an extension of infarct size, and CK release into the coronary vein appeared earlier than in the controls. Dogs receiving nifedipine, 1 /ig/kg, showed a 12% fall in blood pressure, no rise in heart rate, an improvement in regional perfusion, and ECG signs that suggested limitation of infarct size. There also was delayed release of coronary venous CK. The effects of nifedipine on the natural history of regional myocardial perfusion, the electrocardiogram, and enzyme release from the heart were dose related and cannot be generalized. These observations warrant further clinical investigation to improve the use of this agent in man. Circ Res 44: 16-23, 1979 THE extent of ischemic myocardial damage during acute myocardial infarction is one of the important determinants of morbidity and mortality. Recent studies have encouraged a search for interventions that can affect the balance between energy supply and demand during acute infarction of the heart (Maroko et al., 1971; Braunwald andMaroko, 1974). Nifedipine (4-(2'-nitrophenyl)-2,6-dimethyl-l,4-dihydropyridine-3,5-dicarboxylic acid dimethyl ester) has been shown to retard the transmembrane influx of calcium into ischemic myocardial cells, increase coronary blood flow, delay ischemic contracture, and preserve myocardial creatine kinase activity (Henry, 1975;Fleckenstein, 1975;Vater, 1975;Schmier et al., 1975). These combined pharmacological properties suggest that a favorable effect on acutely ischemic myocardium may be possible.The purpose of this study was to observe the changes of regional myocardial perfusion, the epicardial ECG, and the appearance of creatine kinase activity in coronary venous blood in dogs during the 5 hours following occlusion of the left anterior descending coronary artery (LAD). The dose-related effects of nifedipine on these parameters were measured, and the use of this drug to protect the ischemic myocardium is discussed. MethodsTwenty-five mongrel dogs weighing 30-55 kg were anesthetized with intravenous sodium thiopental (Pentothal, 12 mg/kg). Respiration ...

Concern has been expressed about the relatively high radiation doses to the lens of the eye received by the operator during cardiac catheterization studies. A study was undertaken to assess the occupational doses received by cardiologists and to examine the factors that affect the individual's eye dose. Eighteen cardiologists working in five catheterization laboratories at three centres were included in the study. Their eye doses, workload and individual study details were monitored at each centre. Operating dose rates and scattered radiation were also measured for each unit to compare equipment performance. The study demonstrated that the relationships between the cardiologist's eye dose and factors such as the dose efficiency of the X-ray equipment, scattered dose rates, examination protocols and workload are complex and vary from centre to centre. Because of these variations general workload limits may be inaccurate and should only be used for general guidance when no direct measurements are available. Such limits should be verified by local measurements as soon as is practical.

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Implantable cardioverter defibrillators (ICDs) reduce sudden arrhythmic death risk but when these devices are programmed DDD and pace in the right ventricle (RV), they can be associated with increased mortality and heart failure morbidity compared to an ICD programmed to back-up RV. An ideal ICD would provide effective treatment for life-threatening tachyarrhythmias, reduce unnecessary RV pacing and maintain AV synchrony. The Inhibition of Unnecessary RV Pacing with AV Search Hysteresis (AVSH) in ICDs (INTRINSIC RV) study will assess whether an ICD programmed to DDDR with AVSH is equal to an ICD programmed to VVI with regard to mortality, heart failure hospitalizations, and several predefined secondary enpoints. AVSH allows intrinsic AV conduction beyond the programmed AV delay to help minimize ventricular pacing. INTRINSIC RV, a multi-center, randomized, prospective trial will enroll >1,200 participants who receive a Guidant VITALITY AVT ICD. ICDs are programmed initially to DDDR AVSH 60-130. Then, after a week, if the %RV pacing <20%, patients are randomized to VVI-40 or DDDR 60-130 with AVSH. Those with RV pacing > or =20% are placed in an obvservational arm and programmed ad libitum by the treating physician. Patients are followed for one year. This large, randomized, controlled, clinical trial will address whether DDDR with AVSH programming is equivalent to VVI programming in an ICD with regard to mortality and heart failure hospitalization.

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The Activation of mechanoreceptors by bulging of the ischemic area12,13 has also been proposed as a mechanism potentially responsible for cardiac pain. To check this hypothesis, we have explored the possibility that the magnitude or the rate of change of left ventricular volume during acute myocardial ischemia, or a combination of these parameters, could account for the presence or absence of anginal pain.