Myocardial kinetics of thallium and potassium in man.
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Biomedical subjects
Publications and source records attributed to A Biagini.
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To investigate the pathogenesis of myocardial infarction we undertook a systematic study of patients with angina at rest, a syndrome known to evolve frequently into infarction. Among 187 consecutive patients, 37 had infarction, all in the area that showed electrocardiographic changes during angina. In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented. In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks. One patient in whom spasm was observed at the onset of infarction died six hours later; at post-mortem examination, a fresh laminar thrombus was found at the site of the spasm. After infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiography.
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Coronary angiography was performed during 34 angina attacks in thirty patients admitted because of recurrent angina at rest. Nineteen (seventeen with S-T segment elevation and two S-T depression) had angiograms during a spontaneous attack, eleven (nine with S-T elevation and two with S-T depression) during an attack induced by intravenous ergonovine maleate. Control coronary angiograms showed a wide range of atherosclerotic obstruction, from normal vessels to severe triple-vessel disease. During the anginal attack, all patients with S-T segment elevation had vasospasm localised to one of the major branches, often resulting in complete occlusion. Attacks with S-T segment depression were seen only in patients with double or triple vessel disease, and here the vasospasm generally affected coronary branches without causing complete occlusion. When appropriately searched for, vasospastic angina seems to be common.
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We have investigated whether vasospastic anginal attacks might be associated with myocardial cell damage even when permanent ORS or ST-T changes are absent. We obtained serum time-activity curves of creatine kinase MB, of myoglobin, and of alpha hydroxybutyrate dehydrogenase in 15 patients with vasospastic angina admitted to our Coronary Care Unit (CCU). A slight but consistent rise and fall of both myoglobin and creatine kinase MB was observed in 7 patients (4 presented a definitive myocardial uptake of 99mTc pyrophosphate, and I had a faint deposition). A similar pattern was observed for myoglobin alone in 3 patients (1 presented a negative myocardial scan), while no consistent changes were found in the remaining 5 patients (2 presented a faint deposition of 99mTc pyrophosphate). No significant change of alpha hydroxybutyrate dehydrogenase was observed in any of the patients. The coherent rise and fall of the levels of myocardial cytosolic components after prolonged episodes of vasospastic angina suggests that cell damage may occur even in the absence of persistent QRS and ST-T changes.
Variation in cyclic (systolic-to-diastolic) echodensity has been demonstrated to be a reliable index of preserved myocardial function. Paradoxic septal motion can be observed frequently after cardiac surgery in the absence of any functional impairment. The aim of the study was to evaluate whether regional cycle-dependent gray-level variation in the septum is affected by abnormal septal motion after cardiac surgery. Ten patients undergoing cardiac surgery for coronary artery bypass grafting were evaluated by continuous transesophageal echocardiographic monitoring from the transgastric approach, both before and after surgery. In each patient septal motion was assessed qualitatively as normal or paradoxic. Images were digitized off-line and cyclic gray-level variation was measured in each patient by means of dedicated software. By selection, all patients exhibited normal septal motion and thickening at baseline. After surgery, five patients showed a paradoxic septal motion (group I), whereas in the remaining five patients (group II) septal motion remained normal. Percent area change, measured with the floating center-of-mass reference system, was similar in the two groups both before (I = 42% +/- 7% versus II = 44% +/- 13%; difference not significant) and after surgery (I = 39% +/- 8% versus II = 40% +/- 1%; difference not significant). Cyclic gray-level variation was also similar in the two groups, both at baseline (group I = 61% +/- 16% versus group II = 68% +/- 18%; difference not significant) and after surgery (50% +/- 13% versus 57% +/- 16%; difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac pain is a key symptom for diagnosis of myocardial ischemia in man, even if a minority of transient myocardial ischemic episodes are painful. A multiparametric monitoring approach - associating non-invasive and invasive monitoring techniques during transient myocardial ischemia with and without pain - allows to achieve a clinical diagnosis and obtain information about the pathophysiology of the anginal syndrome.
The clinical recognition of the cardiac origin of chest pain or discomfort on the basis of the description made by the patient, is often difficult. Nevertheless, considering the importance of the correct diagnosis of such syndrome, much work has been done in this field. In this report we will comment data from the literature and from our own, on the quality, duration, irradiation and on the precipitating or relieving factors that are more frequently associated with anginal pain.
In 40 drug-free patients 2052 episodes of transient myocardial ischemia (28% painful) were recorded by 24-h ambulatory ECG. Pain was more frequently associated with longer duration of ischemia and greater ST segment shift and with the presence of ventricular arrhythmias within the ischemic episode. Heart rate always showed a growing trend during the ischemic episode. Circadian distribution of painless ischemic episodes showed a maximum peak at 2 a.m. while the most painful attacks occurred early in the morning (6 a.m.).
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