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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been reported that intraaortic balloon pumping can prevent reocclusion after coronary angioplasty for acute myocardial infarction. The speculated mechanism has been the production of markedly enhanced diastolic coronary perfusion pressure; however, most studies have reported that intraaortic balloon pumping has little effect on coronary blood flow. To assess the effectiveness of this procedure, we studied 12 patients with acute anterior myocardial infarction who were undergoing coronary angioplasty and intraaortic balloon pumping. After successful angioplasty, coronary blood flow velocity was measured with a coronary Doppler catheter before and during intraaortic balloon pumping. Although mean coronary blood flow velocity was unchanged, intraaortic balloon pumping increased peak coronary blood flow velocity from 34.6 +/- 5.0 cm/sec (mean +/- SEM) to 46.7 +/- 5.8 cm/sec (p < 0.005). Such an increase in peak coronary blood flow velocity seemed to be a mechanism by which intraaortic balloon pumping could prevent reocclusion after coronary angioplasty for acute myocardial infarction.
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PMID:Effects of intraaortic balloon pumping on coronary hemodynamics after coronary angioplasty in patients with acute myocardial infarction. 144 77

The authors studied 80 consecutive patients with a first Q wave anterior myocardial infarction (MI) by 2-dimensional and color Doppler echocardiography (echo), on day 3 and day 10 after admission, to determine whether left ventricular (LV) blood flow dynamics differ between those who develop LV thrombus and those who do not. With pulsed Doppler echo, peak flow velocities were measured in diastole at the inflow tract, at the apex in diastole and systole, and at the outflow tract in systole. There were 11 patients (14%) who had LV thrombosis on day 3. On day 10, no other patient developed a thrombus. There was no difference in the Doppler flow velocities, except for lower apical diastolic velocities (0.23 +/- 0.04 m/s) (+/- SEM) in patients with thrombus as compared with those without it (0.33 +/- 0.01 m/s) (p less than 0.05). All patients with thrombus had apical dyskinesis and 8 (73%) had an anteroapical aneurysm, while 40 (58%) patients without thrombosis had dyskinesis and 11 (16%) had an aneurysm (p less than 0.01). The ejection fraction was lower (25.4 +/- 3.2%), the wall motion score was higher (10.6 +/- 0.7), and mitral regurgitation was seen more frequently (45%) in those with LV thrombus (respective values in no thrombus group patients: 32.9 +/- 1.4%, 7.6 +/- 0.3, 7%). The authors conclude that LV thrombus prediction is difficult by Doppler flow velocity study, whereas dyskinesis and aneurysmal dilatation of the LV apex is significantly associated with thrombus.
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PMID:Left ventricular blood flow analysis in patients with and without a thrombus after first Q wave acute anterior myocardial infarction: two-dimensional Doppler echocardiographic study. 157 66

The site of ventricular stimulation is an important variable in the initiation of ventricular tachycardia (VT) by programmed ventricular stimulation. Among 169 patients studied consecutively, 17 (10%) had ventricular tachycardia induced by programmed electrical stimulation from the right ventricular outflow tract but not from the apex. Fourteen of these 17 patients had had prior myocardial infarction (12 had inferior, and two had both inferior and anterior myocardial infarction), two had a dilated cardiomyopathy, and one had a localized cardiomyopathy. Fourteen patients had echocardiograms suitable for analysis. Of these, 12 had posterior/inferior ventricular wall motion abnormalities located at the base of the heart. The ventricular effective refractory periods from the right ventricular outflow tract and right ventricular apex were 237 +/- 4 and 244 +/- 5 msec, respectively (p less than 0.05, mean +/- SEM). Induced VT had a cycle length of 229 +/- 4 msec and had the morphology of right bundle branch block in 12 patients, of left bundle branch block in three patients, and had both morphologies in two patients. In 14 patients the axis was superior. VT was initiated with two extrastimuli in 15 patients and with burst right ventricular pacing in two patients. Similar pacing techniques with identical pacing intervals did not induce VT at the right ventricular apex in 14 of these 17 patients. Further, among the 15 patients whose VT was induced at the right ventricular outflow tract with two extrastimuli, neither burst pacing (n = 13) nor two extrastimuli introduced at faster paced rates (n = 12) induced VT at the right ventricular apex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiologic and anatomic characteristics of ventricular tachycardia induced at the right ventricular outflow tract but not at the apex. 185 27

Pavlovian conditioning was accomplished in two groups of dogs by following a 30-s tone (the CS+) with a short (less than or equal to 1 s) electric shock). An inflatable occluder was implanted around the left circumflex coronary artery in all animals. The CS+ was presented to Group I dogs (n = 6) during control (i.e., no coronary occlusion) and at 30 s and 3 min after the onset of a 4-min left circumflex coronary occlusion. The CS+ evoked a robust increase in heart rate and blood pressure in the control state. A conditional cardiovascular response was still evoked during the acute coronary occlusion despite the evolving myocardial ischemia. No increase in ventricular ectopic beats occurred during the CS+. An anterior myocardial infarction (16.8 +/- 1.7% of left ventricular mass, mean +/- SEM) was created in Group II dogs (n = 8) at the time of surgery. A CS+ was presented, as above, both alone and 1 min after the beginning of a 2-min left circumflex coronary occlusion. There were significant differences in the conditional response in heart rate, left ventricular (systolic) pressure (LVP) and d(LVP)/dt for trials given during the coronary occlusion compared with no occlusion. These dogs were then classified as 'resistant' or 'susceptible' to ventricular arrhythmias approx. 4 weeks later using an exercise and coronary occlusion test. Three of five susceptible dogs, but none of three resistant dogs, evidenced increased severity of arrhythmias during the CS+. We conclude that the nature of the cardiovascular response to behavioral stress during myocardial ischemia depends in part upon the timing of the CS+, the presence or absence of a resident myocardial infarction and the status of the autonomic reflexes controlling the heart.
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PMID:Hemodynamic and arrhythmogenic effects of aversive stress during myocardial ischemia. 234 97

We performed a double-blind randomized trial comparing high doses of subcutaneous heparin (12,500 units every 12 hours) with low doses (5000 units every 12 hours) for 10 days in the prevention of left ventricular mural thrombosis in 221 patients with acute anterior myocardial infarction. Left ventricular mural thrombosis was observed by two-dimensional echocardiography on the 10th day after infarction in 10 of 95 patients (11 percent) in the high-dose group and in 28 of 88 patients (32 percent) in the low-dose group (P = 0.0004). One patient in the high-dose group and four in the low-dose group had nonhemorrhagic strokes (P = 0.17). One patient in the low-dose group had a fatal pulmonary embolism. There was no difference in the frequency of hemorrhagic complications, which occurred in six patients in the high-dose group and four in the low-dose group. The mean (+/- SEM) plasma heparin concentration was 0.18 +/- 0.017 U per milliliter in the high-dose group and 0.01 +/- 0.005 U per milliliter in the low-dose group (P less than 0.0001). In the high-dose group, the mean plasma heparin concentration was 0.10 +/- 0.029 U per milliliter among patients with abnormal two-dimensional echocardiograms, as compared with 0.19 +/- 0.019 U per milliliter among patients with normal echocardiograms (P = 0.01). We conclude that heparin administered subcutaneously in a dosage of 12,500 units every 12 hours to patients with acute anterior transmural myocardial infarction is more effective than a lower dosage (5000 units every 12 hours) in preventing left ventricular mural thrombosis.
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PMID:Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction. 274 63

We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months. No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [+/- SEM] of 21 +/- 8 ml (P less than 0.02) in the placebo group, but by only 10 +/- 6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P less than 0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P less than 0.05). Patients given captopril also had increased exercise capacity (P less than 0.05). This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance.
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PMID:Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. 296 17

Digital subtraction angiography with selective coronary injections of contrast media has enabled us to obtain clear images, not only of the artery, but of the capillary and venous phases of the myocardial perfusion. In the present study, densitometry was used to estimate regional myocardial perfusion dynamics in 10 control cases and 11 anterior myocardial infarction cases. The time density curve showed that contrast material increased rapidly in the arterial phase and appeared to be washed out monoexponentially in the venous phase. The time from the onset of contrast medium injection to the maximal density of the contrast medium (Tp), and the time constant obtained from the washout curve (Tc) were analyzed. In the control group, Tp in the apical region was slightly prolonged as compared with Tp in the anterobasal region, but the difference was not significant (5.2 +/- 0.5 vs 4.2 +/- 0.4 sec: mean +/- SEM). Tc did not definitely change in any portion of the myocardium (anterobasal 5.1 +/- 0.5, anterior 4.8 +/- 0.5, apex 4.6 +/- 0.5 sec, respectively). In anterior myocardial infarction, Tp in the marginal region was significantly prolonged compared to Tp in the control region (6.0 +/- 0.3 vs 4.7 +/- 0.3 sec, p less than 0.01). Tp was prolonged for more than 10 sec in the infarcted region. Tc in the marginal region was markedly prolonged compared to Tc in the control region (7.4 +/- 0.9 vs 4.4 +/- 0.5 sec, p less than 0.025). Tc could not be determined in the infarcted regions because data acquisition time of our apparatus was inadequate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Digital subtraction angiography: image-sequence analysis for regional myocardial perfusion dynamics. 353 55

Infarct size was estimated by cumulative creatine kinase MB isoenzyme (CKMB-r) release and by technetium 99m stannous pyrophosphate (TcPYP) scintigraphy in 27 patients with acute anterior myocardial infarction. In eight patients, scintigraphy showed a central area of reduced tracer uptake surrounded by a peripheral rim of increased TcPYP accumulation ("doughnut" pattern). This appearance occurred only in large infarcts and the maximal scintigraphic area (51.3 +/- 2.8 cm2, mean +/- SEM) in this group was significantly greater than that in the remainder (28.1 +/- 2.5 cm2). Correlation between CKMB-r and maximal scintigraphic infarct area was moderate in the whole group. Exclusion of patients, however, with "doughnut" scintigrams in which correlation was very poor, resulted in substantial improvement in the remainder. It is suggested that in the central regions of large "doughnut" infarcts, reduced blood flow hinders the efflux of CKMB from the centre causing an underestimate of infarct size. Pyrophosphate scintigraphy appears to be more accurate than CKMB release in measuring the size of these large anterior infarcts.
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PMID:Advantages of technetium pyrophosphate scintigraphy over plasma enzyme analysis in estimation of anterior myocardial infarct size. 625 64

The accuracy of three-dimensional transverse section positron emission imaging for quantification of myocardial infarction size was validated and compared with the accuracy of two dimensional planar positron imaging. After induction of acute anterior myocardial infarction in anaesthetised dogs, gallium-68 albumin microspheres were injected into the left atrium. Planar and transverse section images of the thorax were obtained with a multicrystal positron camera. After staining with tetrazolium tetrachloride injected intravenously, the hearts were excised, sectioned manually, and planar imaging repeated. Each myocardial infarction was clearly delineated by transverse section imaging with high contrast ratios (mean 0.68 +/- 0.02 SEM); planar imaging identified seven of nine infarcts but with lower contrast ratios (0.24 +/- 0.04; P < 0.001). The volume of infarcted myocardium determined from transverse section images correlated well with true infarct volume (r = 0.94); whereas planar images poorly predicted infarct size (r = 0.63). Thus, computer-assisted transverse section positron imaging provides in vivo localisation of microsphere distribution for improved radioisotopic quantification of myocardial infarction.
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PMID:Quantification of myocardial infarction by computer-assisted positron emission tomography. 697 82

Changes in hemodynamics and plasma norepinephrine levels during supine bicycle exercise after myocardial infarction were measured to investigate the mechanism of exercise-induced ST-segment elevation. Seventy-eight patients were divided into groups which showed either ST elevation (STE), ST depression (STD), or no ST changes (STU). Most of the STE group had anterior myocardial infarction (90.6%) and single-vessel disease (76.7%). The STE group achieved a significantly higher workload (119.5 +/- 4.0 watts, mean +/- SEM) than the STD group (82.3 +/- 2.8, p < 0.01). Heart rate and cardiac output at maximal workload were significantly higher in the STE group (136.6 +/- 3.4 beats/min, 7.44 +/- 0.28 l/min/m2) than in the STD group (110.0 +/- 3.9, 4.83 +/- 0.36, p < 0.01). Pulmonary artery pressures were less elevated in STE than STD patients. Plasma norepinephrine levels increased significantly at maximal workload in STE patients, as compared to the other groups. In conclusion, the STE group achieved a higher exercise level associated with augmented sympathetic activity, which may be a possible mechanism of exercise-induced ST elevation after myocardial infarction.
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PMID:Exercise-induced ST-segment elevation and hemodynamic responses one month after myocardial infarction. 796 97


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