Role of myocardial ischemia and left ventricular wall motion abnormalities as contributory factors in the genesis of exercise-induced ST-segment elevation in Q-wave myocardial infarction.

In patients with a previous myocardial infarction, controversy exists regarding the significance of postexercise ST-segment elevation in the infarct-related leads. Although usually admitted to be a sign of left ventricular dysfunction or myocardial aneurysm, other studies however have related this finding to transient myocardial ischemia and to the presence of jeopardized but viable myocardium in the infarct area. The aim of the present study was to assess the significance of postexercise ST-segment elevation in Q-wave leads as a marker of transmural ischemia or left ventricular dysfunction in 36 consecutive patients, 16 with exercise-induced ST-segment elevation in infarct-related leads. Patients were evaluated by treadmill exercise testing, coronary angiography and ventriculography, thallium-201 tomographic scintigraphy and radionuclide ventriculography within 3 months of the first myocardial infarction. Sixteen patients (group I) had exercise-induced ST segment elevation and 20 (group II) postexercise inversion, no change or pseudonormalization of the T wave in infarct-related leads. The study showed no difference in infarct-related artery, vessel disease or luminal diameter stenosis in groups I and II. The overall agreement between ST shifts and myocardial perfusion in the infarct area was 30.56% with a kappa coefficient of -0.33 (p = NS). The overall agreement between ST shifts and wall motion abnormalities was 69.44% with a kappa coefficient of 0.39 (p < 0.01), stress-induced ST-segment elevation being associated with severe wall contractile disorders in 85% of the patients. In conclusion stress-induced ST-segment elevation in Q wave leads, although not a marker of wall motion abnormalities, is associated with akinesia or dyskinesia of the left ventricular wall.

Post-exercise electrocardiographic alterations, ST-segment elevation and QTc changes in patients with recent myocardial infarction.

UNLABELLED: Stress-induced ST-segment elevation and a prolongation or no change of the QTc ratio (corrected QT interval for heart rate) at maximal exercise in the infarct leads have been associated with the presence of residual myocardial ischemia in the infarct zone. The aim of this study was to test the agreement between stress-induced ST-segment elevation and post-exercise QTc changes in infarct leads, in 36 consecutive patients, studied by coronariography, radionuclide ventriculography and thallium-201 scintigraphy, within 3 months of the acute myocardial infarction. Sixteen patients (Group I) had exercise-induced ST-segment elevation in the infarct leads and 20 did not (Group II). The study showed no significant difference between severity of vessel disease and occlusion, prevalence of the infarct related artery or left ventricular dysfunction in Group I and II. No agreement between ST-segment shifts and myocardial perfusion in the infarct zone was found. Resting wall motion abnormalities were more severe in Group I than in Group II (p < 0.01). In the total of the 36 patients there was no agreement between ST-segment shifts and QTc-variations. The study showed agreement between QTc changes and myocardial perfusion in the infarct area (K = 0.64) (p < 0.001). CONCLUSION: This study showed no relation between post-exercise ST elevation and post-exercise QTc variations in Q wave leads. QTc variations at the end of exercise in the infarct related leads identified residual ischemia. Exercise ST segment elevation, although not a marker of ischemia, is associated with more severe wall motion abnormalities in the infarct zone.

Comparison between dobutamine echocardiography and thallium-201 scintigraphy in detecting residual stenosis, ischemia, and necrosis in patients with prior myocardial infarction.

BACKGROUND: Following the first attempts to detect myocardial ischemia with two-dimensional echocardiography stress testing, pharmacologic stress using dobutamine infusion has become an alternative to echocardiography exercise testing for evaluation of coronary artery disease. It has been shown that stress echocardiography has a diagnostic accuracy similar to that of an exercise thallium test. Other studies, however, indicated that radionuclide myocardial perfusion imaging was more sensitive than exercise or pharmacologic stress echocardiography for detection of ischemia or jeopardized myocardium. HYPOTHESIS: The aim of the present study was to determine the ability of dobutamine stress echocardiography in comparison with thallium-201 scintigraphy to identify multivessel disease and the presence of myocardial scar and ischemia in 60 consecutive patients who suffered a first myocardial infarction (MI). METHODS: Patients were evaluated by coronary angiography and ventriculography, thallium-201 (201TI) tomographic scintigraphy, and dobutamine echocardiography within 3 months of a first MI. Forty-seven had Q-wave MI and 13 had non-Q-wave MI. Eleven patients were excluded from final analysis-7 because of failure to achieve target heart rate in spite of the use of atropine, and 4 because of high blood pressure following the infusion of dobutamine. RESULTS: Dobutamine echocardiography showed an overall sensitivity of 43% for detection of coronary artery lesions of 50-74% diameter stenosis and 201TI scintigraphy showed a sensitivity of 71%. For detection of lesions of > or = 75% diameter stenosis, dobutamine echocardiography showed a sensitivity of 52% and 201TI a sensitivity of 70%. Overall agreement between wall motion and myocardial perfusion for detection of necrosis and/or ischemia in the infarct area was 40.4% with a kappa coefficient of 0.09 (p = 0.13). For detection of ischemic myocardium outside the infarct zone, overall agreement was 78.6% with a kappa coefficient of 0.49 (p < 0.0001). CONCLUSION: Dobutamine echocardiography results showed a lower sensitivity than myocardial perfusion images in predicting multivessel coronary artery disease, and there was poor agreement between both methods in identifying necrosis or ischemia.

[Coronary artery disease, myocardial perfusion and ventricular function in Q-wave and non-Q-wave myocardial infarcts]. / Doença arterial coronária, perfusão miocárdica e função ventricular em enfartes do miocárdio com onda Q e sem onda Q.

Controversy remains in considering non-Q wave myocardial infarction (NQMI) a distinct pathophysiological entity of Q wave myocardial infarction (QMI). In order to analyze the severity of coronary artery disease, extension of myocardial scar or myocardial ischemia and ventricular function, 78 consecutive patients with QMI and 32 with NQMI, mean age 55.4 +/- 8.5, not submitted to thrombolytic therapy, were studied. Coronary angiography, exercise thallium scintigraphy and radionuclide ventriculography were performed in all at least within 3 months of a prior myocardial infarction. In the present study the occurrence of QMI was significantly more frequent in older patients than NQMI. There was no prevalence of occlusion either in the right, left circumflex or left anterior descending coronary arteries in both groups. Ejection fraction, degree of occlusion and presence of collateral circulation showed an equal prevalence in QMI and NQMI patients. A higher incidence of multivessel disease was found in NQMI that had less necrosis than QMI patients. The prevalence of exercise induced thallium-201 redistribution defects within the infarct zone was substantially higher and involved more scar segments in NQMI patients. Physiological and clinical consequences of coronary thrombosis depends on the size and the number of diseased arteries, the approach the pathophysiologic consequences of coronary disease in terms of fractal structure has been suggested. A pronounced heterogeneity in regional myocardial blood flow in a fractal branching arterial network may be responsible for the pathophysiologic differences of coronary thrombosis between Q-wave and non Q-wave infarction.

Minimal residual coronary obstructions in patients who suffered a first myocardial infarction. A prospective study comparing coronary angiography and exercise thallium scintigraphy.

The purpose of the present study was to correlate the presence of minimal coronary obstruction (< or = 50%) assessed by coronary angiography with the presence of myocardial scar and ischemia detected by thallium-201 myocardial perfusion imaging. The study included 83 consecutive patients (74 men and 9 women) with a mean age 55.4 +/- 8.5 years who suffered a first myocardial infarction and did not undergo thrombolytic therapy. In all patients, coronary angiography, left ventriculography, and exercise thallium-201 tomographic scintigraphy were performed within 3 to 5 months of the myocardial infarction. Coronary arteriograms showed minimal residual obstructions in 37 (45%) patients. Of a total of 54 patients with < or = 50% obstruction, 18 showed persistent defects and 22 reversible defects on thallium scintigrams. The present study showing estimated angiographic stenosis of < or = 50% as being responsible either for myocardial scar or myocardial ischemia on postexercise thallium scintigrams leads us to conclude that percent value of stenosis does not accurately predict the pathophysiologic significance of coronary atherosclerotic lesions in patients who suffer a myocardial infarction. After a first myocardial infarction, coronary angiographies and thallium-201 scintigrams are complementary for an optimal treatment strategy for selected subsets of patients.

Postexercise changes of the QTc interval in patients with recent myocardial infarction.

A lack of the QTc ratio decrease at maximal exercise is considered as an index of exercise-induced ischemia in patients with coronary artery disease. The authors studied 51 patients with recent myocardial infarction in order to evaluate the QTc changes with exercise in assessing the presence of remaining ischemic myocardium. All patients were submitted to exercise stress tests, coronary angiographies, and exercise thallium 201 scintigraphies within 3-5 months of the myocardial infarction. Of the patients studied, 18 showed one-vessel disease and 33 showed multivessel disease. All vessels were classified as patent or occluded. In all patients with reversible thallium 201 defects both at distance and in the infarct zone, the QTc interval following exercise either showed a prolongation or no change from the resting electrocardiogram. In patients with only fixed perfusion defects, the QTc shortened at the end of the test. This study showed a low sensitivity and specificity for inducible ST-segment depression compared with the delayed redistribution on the postexercise thallium 201 scintigram. QTc variations at the end of exercise electrocardiograms are valuable as a noninvasive, low-cost identification of residual ischemic myocardium in patients after myocardial infarction.

Effects of polyoxyethylene-modified superoxide dismutase on reperfusion induced arrhythmias in isolated rat and guinea-pig hearts.

Effects of a newly introduced polyoxyethylene-modified superoxide dismutase (SOD-POE) with prolonged plasma half life (10 h) on reperfusion induced arrhythmias were examined using a 15 min left anterior descending coronary artery (LAD) occlusion followed by reperfusion in the isolated perfused rat and guinea-pig hearts. LAD occlusion was performed by compressing the artery using a suction cup placed on the LAD to which negative pressure was applied. The LAD occlusion was repeated twice at an interval of 20 min. Drugs were infused from 10 min prior to the occlusion to 3 min after reperfusion at either first or second trial of the occlusion and release. ECG was monitored throughout the experiments. In the control group (rat hearts), arrhythmias including ventricular fibrillation (Vf) (incidence, 64.3 to 83.3%), ventricular tachycardia (VT) (66.7 to 84.6%), premature ventricular contraction (PVC) and premature atrial contraction (PAC) occurred immediately after reperfusion and lasted for 1 to 3 min. In both groups treated with SOD-POE (10 U/ml) or native human SOD (10 U/ml), the incidence of Vf and VT was 0% and the number of PVCs significantly decreased. Lidocaine (5 x 10(-7) M, 10(-6) M) also reduced the incidence of VT and the number of PVCs. In guinea-pig hearts, the occlusion and release induced Vf (50%), VT (80%), PVCs and PACs. Both SOD-POE and SOD markedly depressed the incidence of Vf (0%) and VT (14.3% in both groups) and decreased the number of PVCs and PACs. Results demonstrate that SOD-POE has the same pharmacological activity as SOD does in preventing reperfusion induced arrhythmias in isolated rat and guinea-pig hearts, suggesting that it will provide a novel therapeutic approach for preventing oxygen radical-related injury in myocardium and other tissues.

Essential hypertension: a metabolic cause? A hypothesis.

Forty-five hypertensive patients, 28 women and 17 men, age range between 35 and 65 years (mean 50 years), with blood pressures which current therapy did not succeed to control, were submitted to several examinations in order to identify the cause of their hypertension. We found isolated or combined abnormal values of aldosterone, renin, calcium and or potassium as the only alterations in 19 patients. We distinguished 4 groups descretionally classified according to biochemical alterations: renin and aldosterone increase, renin increase, aldosterone increase, calcium and or potassium reduction. The therapy used, intentionally aimed at the correction of the biochemical alterations found. Normal blood pressure was achieved in all patients and simultaneously the biochemical alterations also became normal in patients with isolated hyperreninemia, with combined hyperreninemia and hyperaldosteronemia and in those with hypocalcemia and or hypopotassemia. In patients were only isolated hyperaldosteronemia was found, this condition returned to normal in all except one. We suggest that besides the disturbances in sodium distribution other electrolytes or biochemical alterations may also play an equally important role in regulating, and sustaining essential hypertension.