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    Thrombolytic therapy reduces the incidence of left ventricular thrombus after anterior myocardial infarction - Relationship to vessel patency and infarct size

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    Background Controversial evidence exists as to whether thrombolytic therapy reduces the incidence of left ventricular thrombus in acute myocardial infarction and, if so, how this relates to successful reperfusion. Methods Four hundred and eighteen consecutive patients underwent echocardiography and coronary angiography within 3 weeks of an acute myocardial infarction. A dyssynergic score was calculated by analysing regional wall motion in 18 left ventricular segments. The infarct-related artery was considered patent if TIMI grade 2 or 3 flow and less than 90% stenosis were present. Retrograde perfusion by Rentrop's grade 2 or 3 collaterals was considered significant. Results Large anterior myocardial infarctions were associated with the highest prevalence (39%) of left ventricular thrombosis. Thrombus was also very frequent if the left anterior descending coronary artery was occluded and no collaterals to the infarct area were seen (75%). Anticoagulant therapy reduced the prevalence of left ventricular thrombus, regardless of whether the infarct-related vessel was patent or not. Conversely, in patients undergoing thrombolysis the incidence of left ventricular thrombosis was lower when the left anterior descending coronary artery was patent, and especially when an early creatine kinase peak, suggestive of reperfusion, was recorded (7%). Finally, the presence of left ventricular thrombosis was inversely related to the asynergy score. Conclusion These observations suggest that the presence of left ventricular thrombus is related to the extent of myocardial damage. Thrombolytic therapy reduces thrombus probably by salvaging myocardium at risk

    Exercise-induced T-wave normalization predicts recovery of regional contractile function after anterior myocardial infarction

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    Aims We investigated the ability of T-wave pseudonormalization and ST-segment elevation, which are demonstrated in infarct-related leads during submaximal exercise testing, to predict late recovery of contractile function. Methods We studied 88 consecutive patients (73 males, mean age 59+/-8 years) with anterior infarction, persistent T-wave inversion and a documented lesion of the proximal segment of the left anterior descending coronary artery. They all underwent 2D-echocardiography on admission, 4 weeks as well as 6 months after myocardial infarction to evaluate the dysfunction score and the ejection fraction. Submaximal (75% of maximal predicted heart rate) exercise testing was performed in 80 patients 2 weeks after myocardial infarction following discontinuation of treatment. Results During exercise testing, 59 of the 88 patients showing negative T-waves on the resting electrocardiogram exhibited pseudonormalization (group A) in at least three adjacent precordial leads, whilst 29 (group B) did not. Patients of group A more frequently exhibited an early creatine kinase peak (41% vs 24%, P<0.05) and residual angiographic perfusion (97% vs 69%, P<0.05). The dysfunction score did not change in group B (from 19+/-7 to 22+/-4), but decreased in group A (from 18+/-4 to 11+/-6, P<0.05). The ejection fraction was similar in the two groups on admission (group A: 48+/-7%, group B: 45+/-10%), but was significantly different at 4-week (52+/-99 vs 42+/-11%, P<0.05) and 6-month follow-up (58+/-9 vs 44+/-10%, P<0.01). The concomitant presence of ST-segment elevation and T-wave normalization showed the highest positive predictive value for left ventricular function recovery (100%). Conclusions T-wave normalization induced by submaximal exercise test is frequently associated with residual perfusion to the infarct area and predicts progressive improvement in regional wall motion, especially if associated with ST-segment elevation. Therefore, these electrocardiographic findings may be used as easily obtainable markers of residual viability that predict late recovery in contractile function

    Effects of trimetazidine on metabolic and functional recovery of postischemic rat hearts.

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    The objective of this study was to test the hypothesis that the beneficial effect of trimetazidine during reflow of ischemic hearts is mediated by energy sparing and ATP pool preservation during ischemia. Isolated rat hearts (controls and rats treated with 10(-6) M trimetazidine, n = 17 per group) underwent the following protocol: baseline perfusion at normal coronary flow (20 minutes), low-flow ischemia at 10% flow (60 minutes), and reflow (20 minutes). We measured contractile function, O2 uptake, lactate release, venous pH and PCO2, and the tissue content of high-energy phosphates and their metabolites. During baseline, trimetazidine induced higher venous pH and lower PCO2 without influencing performance and metabolism. During low-flow ischemia, trimetazidine reduced myocardial performance (P = 0.04) and ATP turnover (P = 0.02). During reflow, trimetazidine improved performance (91 +/- 6% versus. 55 +/- 6% of baseline), prevented the development of diastolic contracture and coronary resistance, and reduced myocardial depletion of adenine nucleotides and purines. ATP turnover during low-flow ischemia was inversely related to recovery of the rate-pressure product (P = 0.002), end-diastolic pressure (P = 0.007), and perfusion pressure (P = 0.05). We conclude that trimetazidine-induced protection of ischemic-reperfused hearts is also mediated by energy sparing during ischemia, which presumably preserves the ATP pool during reflow

    PRESERVED VASODILATOR RESPONSE TO ACETYLCHOLINE IN ATHEROSCLEROTIC CORONARY-ARTERIES BEFORE AND AFTER PTCA

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    The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 mu g) and nitroglycerin (200 mu g) on coronary vasular tone. In three patients the protocol was performed at the time of diagnostic coronary angiography and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminal coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post-PTCA segments with residual irregularities, 18 reference segments of the same arteries taken proximal to the stenosis or to the dilatation site, and 11 remote segments of nonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 mu) the agent invariably caused dilatation (9.22 +/- 6.55%), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 +/- 12.82%, P < 0.0001). At the highest doses (50 or 80 mu g) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post-PTCA (-31.54 +/- 10.65%) and stenotic segments (-23.08 +/- 11.88%) than in the reference and remote segments (respectively, -14.88 + 7.63% and -18.67 + 8.37%, P < 0.05). We conclude that: (1) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensitivity; (3) since acetylcholine has direct and endothelium-mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity

    Enoximone echocardiography for predicting recovery of left ventricular dysfunction after revascularization - A novel test for detecting myocardial viability

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    Background-The possibility that enoximone, a nonglycoside, noncatechol, positive inotropic agent, in combination with 2-dimensional echocardiography may predict recovery of myocardial dysfunction after revascularization has not been yet evaluated. Methods and Results-Forty-five patients with chronic coronary artery disease and left ventricular dysfunction underwent dobutamine (DE, 5 to 10 mu g . kg(-1) . min(-1)) and enoximone (EE, 1.5 mg/kg, over 10 minutes) echocardiography. Myocardial wall motion was scored from 1 (normal) to 4 (dyskinesia): an asynergic segment was considered to have contractile enhancement when the score decreased by greater than or equal to 1 grade. Of 478 asynergic segments, 216 (45%) exhibited functional recovery after revascularization. Dobutamine- and enoximone-induced contractile enhancement was observed in 41% and 46% of segments, respectively, Compared with DE, EE had higher sensitivity (88% versus 79%, P<0.01) and negative predictive value (90% versus 84%, P<0.05) in predicting functional recovery. The specificity (89% versus 90%) and positive predictive value (87% for both EE and DE) were similar. Concordant interpretation of EE and DE findings was found in 85% (406 of 478) of affected segments. Prerevascularization coronary angiography showed that stenosis severity of vessels supplying areas which only improved with enoximone was significantly greater (89.9%) than that of vessels (77.7%) supplying areas that responded to both agents (P<0.02), Both dobutamine and enoximone increased heart rate (16% and 10%, respectively), whereas enoximone did not cause changes in systolic blood pressure that increased by 14% with dobutamine. Conclusions-Enoximone echocardiography provides a novel and reliable approach for the prediction of functional recovery after revascularization. Compared with dobutamine echocardiography, the test yields higher sensitivity and induces lesser hemodynamic alterations
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