Biomedical subjects
Publications and source records attributed to S Sclarovsky.
A severe case of flecainide-induced incessant ventricular arrhythmias is presented. These arrhythmias were resistant to various intravenous antiarrhythmic drugs and to cardiac pacing. Intravenous amiodarone administered over a short period and in a high dose strikingly abolished all ventricular arrhythmias.
A 52-year-old man had longstanding hypertension and asymemtric septal hypertrophy and normal major coronary arteries. His acute anterior wall ischemia gave rise to transient Q waves and septoapical dyskinesia, complicated by mural thrombus formation. Follow-up revealed a gradual and complete recovery of echocardiographic left ventricular function with total disappearance of mural thrombi and of electrocardiographic Q waves. Acute myocardial ischemia can cause prolonged electrical and mechanical stunning which can lead to mural thrombus formation.
A patient had repetitive ventricular fibrillation preceded by alternating ST segment depression and elevation. The ECG changes were confined to the precordial leads only, reflecting subendocardial and transmural ischemia, respectively. It is speculated that the patient exhibited consecutive episodes of subtotal and total coronary occlusion, both episodes being critical enough to induce lethal arrhythmias.
The effect of intravenous (IV) amiodarone (300 mg) on heart rate was investigated in 22 patients with acute myocardial infarction (18) or ischemia (4) and sinus tachycardia. There were 11 men and 11 women (age range, 48 to 83 years; mean, 63.5). Amiodarone IV slowed the mean heart rate from 109 +/- 14 beats/min to 94 +/- 15 beats/min (p less than 0.0005). There was a linear correlation between the initial heart rate (preamiodarone) and the final heart rate (postamiodarone), (r = 0.6930, p less than 0.0005). Most of the patients with initial heart rates higher than the mean maintained relatively high heart rates (above the mean), while most patients with lower initial heart rates showed low heart rates (below the mean) after amiodarone administration. Patients in Killip class 1 showed a significant reduction in heart rate after receiving amiodarone, from a mean of 105 +/- 10 to 88 +/- 11 beats/min (p less than 0.01). Patients in Killip class 2 also had reduced heart rates (118 +/- 14 to 81 +/- 39 beats/min), but these changes were not statistically significant. Of the three patients in Killip class 3 to 4, the heart rate slowed by 10 beats/min in one, while in the remaining two no changes were observed. There were no significant side effects from the administration of amiodarone.
The significance of dynamic changes of the QS wave magnitude, as demonstrated in the precordial leads, within the natural evolution of acute anterior wall myocardial infarction (AAMI) was assessed in 25 patients within two weeks of their admission to the intensive cardiac care unit. Two sets of tests, including 12-lead electrocardiogram and a full radionuclear study, were performed in two time periods: (1) within the first 48 hours of admission; and (2) between the 12th and 15th day after admission. Comparison and correlation between the electrocardiographic data, QS waves in leads V2 and V3 and in V1 to V6 (sigma QV2-3 and sigma QV1-6), and radionuclear regional ejection fractions of the noninfarcted posterior muscle (inferior, infero-apical, and posterolateral regions and posterior index) were done. Significant linear correlations were demonstrated between the electrocardiographic variant differences in percentages (sigma QV2-3 and sigma QV1-6) and the radionuclear variant differences, especially the posterolateral and the infero-apical regions, as well as the posterior radionuclear index (r between 0.5 and 0.75; p less than 0.01). In addition, almost all of the patients who showed deepening of QS waves in the precordial leads also showed an increase in regional ejection fractions in uninvolved myocardium, and vice versa. It is concluded that the dynamic changes of the QS wave magnitude in the precordial leads within the evolution of acute anterior myocardial infarction well reflect the changes of the posterior noninfarcted muscle contraction and therefore offers a simple, inexpensive, and indirect electrocardiographic method for evaluating changes in contraction patterns of noninfarcted myocardium.
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This study was undertaken in order to characterize the short-term (1 hour) and long-term (72 hours) effect of dobutamine on hemodynamic and regional ejection fraction parameters measured by radionuclear angiography in patients with chronic congestive heart failure due to coronary artery disease. Baseline hemodynamic and radionuclear parameters were measured and then intravenous dobutamine (8.5 mu/kg/min) was administered. The above parameters were determined again after 1 hour and 72 hours of continuous dobutamine administration. Sixty minutes (short-term) after dobutamine administration heart rate and cardiac index increased significantly (p less than 0.001 for both) and peripheral resistance decreased concomitantly (p less than 0.005). Global left ventricular ejection fraction (LVEF) as measured by multigated equilibrium nuclear angiography (MUGA) increased from 21.8 +/- 10.6% to 25 +/- 13.5 (p less than 0.02). Count-based mean regional ejection fraction in the septal, inferoapical, posterolateral (45 degrees left anterior oblique view) and inferior apical and anterolateral (30 degree right anterior oblique gated first pass) regions increased also. At 72 hours (long-term) after continuous dobutamine infusion, heart rate and cardiac index were still significantly higher and peripheral resistance lower than in the control study. However, global and count-based regional ejection fraction decreased to control values in the right anterior oblique view (first-pass analysis) and the left anterior oblique view (MUGA). Global LVEF measured in the right anterior oblique view by first-pass technique was significantly higher than control in the long-term study (23 +/- 9.7 vs. 27.8 +/- 2.4; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
In this study of 14 patients hospitalized with a first event of myocardial infarction, maximal ST segment depression in precordial leads V2 and V3 was the sole ECG finding during chest pain in the first 24 hours of evolving posterolateral infarction, based upon further two-dimensional echocardiographic examination and cardionuclear imaging. Other ECG findings compatible with posterolateral infarction such as the appearance of Q waves in leads V5 and V6, increased R/S ratio in leads V1 and V2, and a diminution of R wave amplitude in leads 1, aVL, V5, and V6 were relatively delayed manifestations in the majority of patients. The clinical course of all patients was benign. It therefore seems reasonable to conclude that ST segment depression in leads V2 and V3 in the absence of reciprocal ECG changes may represent the initial ECG finding of posterolateral infarction in the suitable clinical context of an acute coronary event.
Time course evolution of R, Q, T and ST components of the electrocardiogram during the first 12 hours of an acute myocardial infarction was studied. A comparison between anterior-extensive and anteroseptal wall infarctions (anterior group), and inferior-extensive and inferior wall infarction (inferior group) showed appearance of significant Q waves within two hours in both groups. R wave loss was nearly a mirror image of Q wave development in both groups. T waves became negative and ST more isoelectric earlier in the inferior than in the anterior group. When combined variations of the four electrocardiographic components were analyzed, four stages of acute infarction were delineated. Stage I--tall R, no Q, ST elevation and positive T; Stage II--significant Q wave appearance; Stage III--negativity of T waves; and Stage IV--ST isoelectric. The inferior group reached stages III-IV within 12 hours; the anterior group remained mostly in stage II. An early appearance of Q waves correlated well with rapid progression to stages III-IV within 12 hours in both infarction groups.
This study was designed to evaluate the effects of metaraminol (Aramine) in six patients with evolving acute inferior wall myocardial infarction accompanied by hypotension and warm limbs. There were 16 episodes of acute inferior wall ischemia, and the response to therapy was judged by evaluating blood pressure and ST segment and T wave abnormalities. Three patients received intravenous isosorbide dinitrate and two received streptokinase as the initial therapy. The mean ST segment elevation was significantly reduced (from 4.94 +/- 1 to 0.5 +/- 0.7 [p less than 0.0001]) after metaraminol infusion was initiated. The average T wave height also decreased (from 6.8 +/- 2 to -1.3 +/- 2.5 mm [p less than 0.0005]). The average heart rate decreased from 82 +/- 11 to 69 +/- 9 beats/min (p less than 0.05) and the mean arterial blood pressure increased from 81 +/- 12 mm Hg before metaraminol treatment to 126 +/- 8 mm Hg after treatment. All these changes occurred within a few minutes after metaraminol therapy was instituted. In 12 episodes, accelerated idioventricular rhythm appeared concomitantly with the resolution of ST segment elevation. Coronary angiography performed between 4 and 10 days after admission demonstrated significant obstruction in all infarct-related arteries, but none was totally occluded. Left ventricular function was normal in three patients and slightly hypokinetic in the inferior wall in two. These results indicate that in a selected group of patients with acute inferior myocardial infarction, metaraminol administration (in certain hemodynamic circumstances) can alleviate acute ischemia within a few minutes and thereby reduce ischemic injury.
The coronary angiographic findings and the in-hospital prognosis of unstable angina pectoris presenting with T wave positivization only (group A: 32 patients) or with additional ST segment elevation (group B: 27 patients) were evaluated. Clinical data and haemodynamic parameters before and during unstable anginal events showed no significant statistical difference, indicating blood flow reduction as the probable mechanism of ischaemia in both groups. The incidence of hospital myocardial infarction was higher in patients of group B (group A 6.24% vs group B 31%; P less than 0.02). Death due to haemodynamic deterioration occurred in 2 patients of group B. This finding can be partially explained by more developed collateral circulation in patients with T wave changes only (25 of 65 obstructed arteries in group A vs 8 out of 48 obstructed arteries in group B; P less than 0.05). Left ventricular function was comparable between the two groups. The extent, severity and location of coronary artery disease was similar in the groups. Thus, the electrocardiographic pattern of T wave changes only, in patients with unstable angina pectoris (group A) define a subgroup who have a favourable prognosis and development similar to patients with chronic stable angina pectoris. Urgent measures may be delayed in this group.
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We retrospectively evaluated 32 patients with unstable angina (UA) and no evidence of increased oxygen demand during episodes of chest pain (no significant changes in heart rate and blood pressure), who developed an acute myocardial infarction (AMI) during the same hospitalization. Based on the type of ST changes during anginal pain, two groups were defined: Group A included 19 patients who developed ST elevation during AMI; 15 of these 19 patients (79%) were in Killip class I, two were in class II, and there was one patient each in classes III and IV, respectively. Only one of the 19 patients died. Group B included 13 patients who developed ST depression during AMI; nine of these 13 patients were in Killip class IV and the remaining four patients died before they could be evaluated. Ten patients died (77%) (p less than 0.01), seven in electromechanical dissociation and three in cardiogenic shock. Postmortem examination, performed in four patients, revealed total obstruction of the left main coronary artery. It is concluded that patients with UA who, during attacks of chest pain, develop ST depression and no evidence of increased oxygen demand may have a poor prognosis when they develop an AMI. This selected group of high-risk patients appears to need immediate intensive medical care and most probably early surgical treatment.
We evaluated 46 patients with unstable angina (UA), who showed no significant changes in heart rate, blood pressure, and double product (as evidence of increased oxygen demand) during episodes of chest pain. Coronary angiography was performed in all patients during the same hospitalization. Of 26 patients with UA and ST depression (group A), 10 had left main coronary artery disease (CAD) and eight had left main equivalent CAD. Of 20 patients with UA and ST elevation (group B), only one had left main CAD and one had left main equivalent CAD. All patients in group A had ST depression in leads V4 and V5, and all patients in group B had ST elevation in leads V2 and V3. The presence of ST depression in leads V4 and V5 in UA patients without evidence of increased oxygen demand may be suggestive of significant left main or left main equivalent CAD. Therefore, coronary angiography is recommended during the same hospitalization.
In search of a simple method for potential evaluation of leukocyte aggregation in states of infarction, we compared the leukergy test, which consists of leukocyte aggregation visualized in a peripheral blood test, to the neutrophil aggregation activity (NAA) test, which consists of in vitro aggregation of neutrophils from normal donors by a patient's plasma. Seventy-five patients participated in the study; 20 with ischemic heart disease and no infarction, 41 with relatively small myocardial infarctions, and 14 with large myocardial infarctions, the respective values of leukergy being 6.9 +/- 3.2, 10.8 +/- 4.6, and 20.5 +/- 14%. On the other hand, neutrophil aggregation activity was the same in a group of 10 patients without myocardial infarction and 10 with myocardial infarction. In these two groups, which showed no difference in the NAA test, the respective leukergy values were 4 +/- 1.5 and 21.7 +/- 10.6%. Thus leukergy correlates better with the clinical picture than does the NAA test.
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In a patient with the sick sinus syndrome and near syncope a prolonged sinus pause was documented and reproduced thereafter during sustained deep inspiration. Administration of intravenous atropine abolished this phenomenon, most probably indicating a hyperresponsiveness of the sinus node and AV junction to a vagotonic reflex.