[Role of thrombosis and coronary vasospasm in etiology of myocardial infarction].
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Animals↗
Biomedical subjects
H Tomoike
Publications and source records attributed to H Tomoike.
Heterogeneous myocardial distribution of iodine-123 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) in patients with hypertrophic cardiomyopathy.
IT has been proposed that iodine-123 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (123I-BMIPP) is an agent for myocardial fatty acid metabolism in animal models. The aim of the present study was to determine whether alterations in fatty acid uptake and/or utilization in patients with hypertrophic cardiomyopathy (HCM) could be detected by 123I-BMIPP. Myocardial imaging with 123I-BMIPP and thallium-201 (201Tl) was performed in 14 fasted patients. A dose of 111 MBq of 123I-BMIPP was administered intravenously at rest, and myocardial emission computed tomography was obtained 20 min and 3 h after injection. The 201Tl imaging was also performed within 1 week after the 123I-BMIPP study. The regional myocardial uptake and clearance of 123I-BMIPP and 201Tl were assessed quantitatively. The myocardial distribution of 123I-BMIPP was more heterogeneous than that of 201Tl in patients with HCM. The myocardial uptake of 123I-BMIPP was lower in the anteroseptal region of the left ventricle than in the posterolateral region (74% vs. 85%, P less than 0.001). The anteroseptal wall showed a faster clearance of 123I-BMIPP than the posterolateral wall (33% vs. 27%, P less than 0.01). Both a decreased uptake and rapid clearance of 123I-BMIPP were observed in the hypertrophied myocardium of the anteroseptal wall, where 201Tl uptake was normal or even increased. Myocardial segments with a markedly increased thickness showed a lower uptake and faster clearance of 123I-BMIPP than those with mild hypertrophy (uptake 73% vs. 82%, P less than 0.05; clearance 30% vs. 25%, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiomyopathy, Hypertrophic↗
Recombinant tissue-type plasminogen activator ameliorates ischemic derangements induced by thrombotic occlusion in closed chest anesthetized dogs.
Effects of thrombotic coronary occlusion followed by thrombolytic reperfusion with recombinant tissue-type plasminogen activator (rt-PA) on infarct size and left ventricular function were studied in anesthetized closed chest dogs. After thrombotic occlusion of the left anterior descending coronary artery was produced by a copper coil technique, 74 dogs were randomly alloted to three groups; dogs treated with rt-PA at 90 min (n = 23) (group I) and at 180 min (n = 25) (group II) of the thrombotic occlusion, and 26 dogs treated with saline solution (permanent thrombotic occlusion, group III). The loading dose of intravenous rt-PA was 8,160 IU/kg body weight per min at the initial 60 min and the maintenance dose was 2,450 IU/kg per min continuously infused for 24 h. Thrombolytic recanalization was achieved at 15 +/- 4 and 18 +/- 6 min after rt-PA infusion in groups I and II, respectively. Infarct size and area at risk were determined by triphenyltetrazolium chloride staining and postmortem angiography; infarct size/area at risk ratio was 10 +/- 3% (n = 10), 33 +/- 7% (n = 9) and 63 +/- 3% (n = 10) in groups I, II and III, respectively (difference significant among groups). To examine whether infarct size and left ventricular function after thrombolytic reperfusion differ from those after mechanical reperfusion, 39 other dogs (group IV) underwent mechanical coronary occlusion for 106 +/- 1 min (occlusion period comparable with that of group I) and reperfusion using a balloon catheter.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia↗
Glibenclamide decreases basal coronary blood flow in anesthetized dogs.
The effects of ATP-sensitive K+ channel blockade on coronary blood flow were studied in 13 anesthetized open-chest dogs. A specific ATP-sensitive K+ channel blocker, glibenclamide, was infused into the left circumflex coronary artery (LCx). Coronary blood flow of LCx and systolic segment shortening at the LCx area were measured. Intracoronary infusion of glibenclamide (0.5, 5, and 50 micrograms.kg-1.min-1) decreased coronary blood flow dose dependently. Glibenclamide at the dose of 50 micrograms.kg-1.min-1 decreased LCx coronary blood flow by 55 +/- 4% (P less than 0.01), which was accompanied by a decrease in percentage segment shortening at the LCx area (P less than 0.01) and ST elevation. When coronary blood flow was maintained at the baseline level by simultaneous infusion of sodium nitroprusside (1-3 micrograms/min ic) or pinacidil (0.3-0.6 mg/min ic), glibenclamide did not alter percentage segment shortening or produced ST elevation. The latter results suggest that glibenclamide decreased coronary blood flow, which secondarily induced myocardial ischemia and dysfunction. Our results suggest that ATP-sensitive K+ channels of coronary arteries are involved in maintaining the level of resting coronary blood flow under physiological conditions in anesthetized dogs.
Animals↗
Relation between recovery sequence estimated from body surface potentials and T wave shape in patients with negative T waves and normal subjects.
BACKGROUND: Advances in analytical methods of the epicardial electrical potentials allowed us to demonstrate spatial distributions of local recovery. Because local recovery will be reflected in events on body surface ECG mapping, abnormalities in recovery sequence that may be responsible for the origin of negative T waves can be detected from body surface potentials. METHODS AND RESULTS: Eighty-seven unipolar ECGs were recorded simultaneously from the entire thorax in patients having negative T waves on left anterior precordial leads and in normal subjects. These included 40 patients with anterior myocardial infarction (MI), 21 patients with left ventricular hypertrophy (LVH), and 44 male volunteers. We measured Tmax time, defined as the instant of maximal first derivative of the T wave as the index of local recovery (Wyatt's method). Parameters related to T wave potentials were positive T wave amplitude, negative T wave amplitude, and T integral. Significant correlations were observed between the Tmax time and each of the T wave potentials. The T wave potentials were dependent on Tmax times. In the anterior MI, the late Tmax times were located on the upper left anterior chest and early Tmax times on the lower right lateral chest. In the LVH, the area showing a delayed recovery was displaced in a left downward direction compared with anterior MI. CONCLUSIONS: Body surface Tmax time distributions clearly separate two negative T wave groups, i.e., anterior MI and LVH. Appearance of the negative T waves correlates well with the presence of the area with delayed Tmax time on the spatial distribution.
Adult↗
Spectral analysis of 87-lead body surface signal-averaged ECGs in patients with previous anterior myocardial infarction as a marker of ventricular tachycardia.
BACKGROUND: There were few studies on the relation between the body surface distribution of high- and low-frequency components within the QRS complex and ventricular tachycardia (VT). METHODS AND RESULTS: Eighty-seven signal-averaged ECGs were obtained from 30 normal subjects (N group) and 30 patients with previous anterior myocardial infarction (MI) with VT (MI-VT[+] group, n = 10) or without VT (MI-VT[-] group, n = 20). The onset and offset of the QRS complex were determined from 87-lead root mean square values computed from the averaged (but not filtered) ECG waveforms. Fast Fourier transform analysis was performed on signal-averaged ECG. The resulting Fourier coefficients were attenuated by use of the transfer function, and then inverse transform was done with five frequency ranges (0-25, 25-40, 40-80, 80-150, and 150-250 Hz). From the QRS onset to the QRS offset, the time integration of the absolute value of reconstructed waveforms was calculated for each of the five frequency ranges. The body surface distributions of these areas were expressed as QRS area maps. The maximal values of QRS area maps were compared among the three groups. In the frequency ranges of 0-25 and 150-250 Hz, there were no significant differences in the maximal values among these three groups. Both MI groups had significantly smaller maximal values of QRS area maps in the frequency ranges of 25-40 and 40-80 Hz compared with the N group. The MI-VT(+) group had significantly smaller maximal values in the frequency ranges of 40-80 and 80-150 Hz than the MI-VT(-) group. These three groups were clearly differentiated by the maximal values of the 40-80-Hz QRS area map. CONCLUSIONS: It was suggested that the maximal value of the 40-80-Hz QRS area map was a new marker for VT after anterior MI.
Electrocardiography↗
Mechanism of ergonovine-induced hyperconstriction of the large epicardial coronary artery in conscious dogs a month after arterial injury.
This study investigated the mechanism of ergonovine-induced hyperconstriction of coronary artery in conscious dogs that had undergone endothelial denudation one month earlier. The diameter of the large epicardial coronary artery was continuously measured by a sonomicrometer in 12 dogs in which two pairs of 10-MHz piezoelectric crystals had been surgically implanted at the denuded and nondenuded sites of coronary arteries. A month after the endothelial denudation, intravenous ergonovine (0.01, 0.1, 0.3, and 1.0 mg) produced transient dilation followed by dose-dependent constriction. The degrees of dilation were comparable between the denuded and nondenuded sites. The magnitudes of constriction induced by ergonovine were significantly larger in the denuded site than in the nondenuded site: the percent reductions in diameter evoked with 0.3 mg ergonovine were 14.4 +/- 2.3% and 3.8 +/- 0.8% (p less than 0.01) at the denuded and nondenuded sites, respectively. The magnitudes of constriction induced by intravenous phenylephrine (0.02, 0.06, and 0.2 mg) were comparable in the denuded and nondenuded sites. Methysergide (a nonselective serotonergic blocker) in a dose of 0.5 mg/kg significantly inhibited vasoconstriction induced by ergonovine (0.3 mg) from 13.1 +/- 1.1% to 2.7 +/- 1.0% (p less than 0.01) at the denuded site and from 4.2 +/- 0.6% to 0.8 +/- 0.3% (p less than 0.05) at the nondenuded site. Diltiazem (1.0 mg/kg) selectively inhibited the ergonovine-induced hyperconstriction. Ketanserin (0.5 mg/kg), prazosin (1.0 mg/kg), or indomethacin (5.0 mg/kg) did not prevent the ergonovine-induced hyperconstriction. Histological study revealed intimal thickening and regenerated endothelium in the denuded site.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Coronary spasm and integrity of endothelial function.
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Animals↗
Dipyridamole electrocardiography test for the assessment of the severity of coronary artery disease.
The purpose of this study was to investigate the relationship of dipyridamole-induced ST changes to the severity of coronary artery disease. The subjects were 100 patients without myocardial infarction who underwent coronary arteriography for the diagnosis of coronary artery disease. The dipyridamole injection test (D) (0.568 mg/kg/4 min), and symptom-limited treadmill exercise test (T) were performed separately. Body surface electrocardiographic mapping of 87 leads was performed in both tests. The incidences of significant ST depression greater than or equal to 0.10 mV, number of leads showing significant ST depression (nST) and the maximal voltage of ST depression (maxST) in D and T were compared to the number of diseased coronary arteries. In patients without significant coronary stenosis (0VD group), the incidence of ST depression in the dipyridamole test was significantly lower than that in the treadmill test (D 9% vs T 47%, p less than 0.01). While, in one vessel disease (1VD), two vessel disease (2VD), and three vessel disease (3VD) groups, there was no significant difference in the incidence of ST depression between the dipyridamole test and the treadmill test (in 1VD, D 44% vs. T 65%; in 2VD, D 67% vs. T 93%; and in 3VD, D 93% vs. T 96%). In the dipyridamole test, nST was 0.6 +/- 2.4 in 0VD, 4.5 +/- 6.9 in 1VD, 4.1 +/- 4.5 in 2VD, and 10.6 +/- 8.1 in 3VD. Significant differences were found between 0VD and 1VD (P less than 0.05), 0VD and 3VD (P less than 0.01), 1VD and 3VD (P less than 0.01), and 2VD and 3VD (p less than 0.01). The maxST in the dipyridamole test was 0.02 +/- 0.04 mV in 0VD, 0.10 +/- 0.12 mV in 1VD, 0.13 +/- 0.11 mV in 2VD, and 0.22 +/- 0.11 mV in 3VD. Significant differences were found between 0VD and 1VD (p less than 0.01), 0VD and 2VD (p less than 0.01), 0VD and 3VD (p less than 0.01), 1VD and 3VD (p less than 0.01), and 2VD and 3VD (P less than 0.01). For the diagnosis of 3VD, the dipyridamole ECG test had as high a sensitivity (93% vs 96%), higher specificity (68% vs 38%, p less than 0.01), and higher predictive accuracy (75% vs 54%, p less than 0.01) than the treadmill test.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
[Vascular endothelial function in coronary artery spasm].
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Animals↗
[Thallium-201 myocardial perfusion imaging during adenosine-induced coronary vasodilation in patients with ischemic heart disease].
201Tl myocardial perfusion imaging during adenosine infusion was performed in consecutive 55 patients with suspected coronary artery disease. Adenosine was infused intravenously at a rate of 0.14 mg/kg/min for 6 minutes and a dose of 111 MBq of 201Tl was administered in a separate vein at the end of third minute of infusion. Myocardial SPECT imaging was begun 5 minutes and 3 hours after the end of adenosine infusion. For evaluating the presence of perfusion defects, 2 short axis images at the basal and apical levels and a vertical long axis image at the mid left ventricle were used. The regions with decreased 201Tl uptake were assessed semi-quantitatively. Adenosine infusion caused a slight reduction in systolic blood pressure and an increase in heart rate. The rate pressure products increased slightly (9314 +/- 2377 vs. 10360 +/- 2148, p < 0.001). Chest pain (24%) and headache (13%) were the frequent side effects. The second-degree atrioventricular block was developed in 11 of 55 (20%) patients. All symptoms and hemodynamic changes were well tolerated and disappeared within 1 or 2 minutes after discontinuing adenosine infusion. The sensitivity and specificity for the detection of patients with coronary artery disease were 100% (31/31) and 88% (7/8), respectively. 201Tl myocardial imaging during adenosine infusion was considered to be safe and useful for evaluating the patients with ischemic heart disease.
Adenosine↗
[A case of acute isolated (Fiedler's) myocarditis diagnosed by histopathological study with rapid unfortunate course].
A 65 year-old-man was admitted to our hospital complaining of orthopnea and precordial oppressive feeling. Chest roentgenogram revealed congestive heart failure. Electrocardiogram revealed acute myocardial infarction-like pattern. Serum enzymes (CPK, GOT, LDH) were slightly elevated, but serum antiviral antibodies were not elevated. Echocardiogram showed severe symmetrical left ventricular (LV) hypertrophy, but there was no abnormality of LV wall motion. He died of progressive heart failure and ventricular fibrillation on the second hospital day. A necropsy was performed within one hour of death. The heart was enlarged (690 g) with both left and right ventricular hypertrophy. The myocardium disclosed a diffuse infiltration predominantly of eosinophilic leucocytes. Histopathological study revealed giant cell formation and granulomatous lesions in the myocardium. There was no overt endocarditis or pericarditis. We concluded that the severe LV hypertrophy was due to myocardial inflammatory swelling. From these findings, we diagnosed this case as acute isolated (Fielder's) myocarditis.
Acute Disease↗
Effects of endothelin-1 on epicardial coronary tone, coronary blood flow, ECG-ST change and regional wall motion in anesthetized dogs.
The effects of intracoronary-administrated endothelin-1 on coronary hemodynamics and regional myocardial function were studied in anesthetized open-chest dogs. Epicardial coronary diameter (CoD) and coronary blood flow (CBF) were measured by a sonomicrometer of 10 MHz piezoelectric crystals and an electro-magnetic flow probe on the left circumflex coronary artery (LCX). Regional wall motion was sonomicrometrically measured at regions supplied by the LCX and left anterior descending artery (LAD) and electrocardiograms were recorded. Endothelin-1, administered as a bolus injections into the LCX via an intracoronary cannula, in a dose-dependent manner reduced COD and CBF. The extent of the reduction of COD and CBF at a dose-dependent manner reduced COD and CBF. The extent of the reduction of COD and CBF at a dose of 300 pmol was 12.3 +/- 1.5% (P less than 0.01) and 86 +/- 5% (P less than 0.01), respectively, of the control. The extent of CBF reduction and deterioration of systolic wall motion were linearly related with the dosage of endothelin-1. ST-elevation (lead II) and fatal ECG abnormalities, including complete atrioventricular block or ventricular fibrillation, were observed with doses above 60 and 100 pmol, respectively. Coronary angiography revealed that filling defects of dye were propagated from the third or distal branches to those of more proximal arteries when the doses of endothelin-1 were cumulatively infused into the LCX. Accordingly, lethal myocardial ischemia induced by endothelin-1 is produced by critical obstruction of rather small coronary vessels.
Animals↗
Putative mechanisms of the impairment of endothelium-dependent relaxation of the aorta with atheromatous plaque in heritable hyperlipidemic rabbits.
Attenuation of acetylcholine-induced endothelium-dependent relaxation of thoracic aortas excised from Watanabe heritable hyperlipidemic (WHHL) rabbits linearly correlated with the percent area coated with atheromatous plaque. To elucidate mechanisms related to this reduced endothelium-dependent relaxation in the presence of atherosclerosis, the acetylcholine-induced release of endothelium-derived relaxing factor (EDRF) was assessed functionally as a percent relaxation of the precontracted detector strips obtained from the tunica media beneath the intact intima or the atheromatous plaque in the same aortic ring preparation. Relaxations of the normal detectors to effluents containing EDRF of thoracic aortas during stimulation by acetylcholine (3 x 10(-6) M) in heterozygous and homozygous WHHL rabbits were 73 +/- 5% and 59 +/- 9% (p less than 0.01) of the phenylephrine-induced precontraction, respectively. Relaxations of the atherosclerotic detectors to effluents (EDRF) through the aortas during stimulation by acetylcholine (3 x 10(-6) M) in heterozygous and homozygous WHHL rabbits were 16 +/- 4% and 14 +/- 5%, respectively--values significantly smaller than those seen in the normal detectors. When superoxide dismutase was added to the perfusate of the donors from homozygous and heterozygous WHHL rabbits, atherosclerotic detectors relaxed by effluents stimulated by acetylcholine to 73% and 65% (p less than 0.01 versus before the addition of superoxide dismutase) of the normal detector, respectively. Relaxations induced by sodium nitroprusside as well as the contractions by acetylcholine, phenylephrine, and KCl (118 mM) were comparable in detector strips from the normal and atherosclerotic portions. Thus, not only is the amount of EDRF released by acetylcholine reduced in the presence of atherosclerosis, the tunica media beneath the atheromatous plaque is also to some extent responsible for the superoxide-induced inactivation of EDRF.
Acetylcholine↗
Effects of synthetic human atrial natriuretic peptide on the human coronary circulation in subjects with normal coronary arteries.
Atrial natriuretic peptide (ANP) is recognized as an "endogenous vasodilator". The purpose of this study was to determine the effects of a clinical therapeutic dose of synthetic alpha-human ANP on the coronary circulation in 15 subjects with normal coronary arteries and normal ventricular function. The epicardial coronary arterial diameter was measured by selective coronary arteriography. Coronary blood flow was estimated from the arterial cross-sectional area and the flow velocity determined using an subselective intracoronary Doppler catheter. ANP, 0.03 micrograms/min/kg given intravenously over 15 minutes, caused a dilation of the large epicardial coronary artery (n = 8): the diameter of the proximal left anterior descending artery dilated from 2.6 +/- 0.4 to 3.1 +/- 0.5 mm (p less than 0.01). Mean arterial pressure decreased from 89 +/- 5 to 83 +/- 5 mmHg (p less than 0.01); heart rate did not change during ANP infusion. Estimated coronary blood flow significantly increased (n = 6, p less than 0.01), and thus the coronary vascular resistance decreased after ANP infusion, suggesting an ANP-induced dilation of resistance vessels. The present study demonstrates that in human subjects a clinical dose of ANP by intravenous infusion dilates both the large epicardial and small resistance coronary vessels. These results suggest a potentially beneficial role for ANP in reducing the severity of myocardial ischemia in patients with ischemic heart disease.
Adult↗
Simultaneous assessment of left ventricular wall motion and myocardial perfusion at rest and during exercise by technetium-99m methoxy isobutyl isonitrile.
First-pass radionuclide ventriculography followed by myocardial SPECT with technetium-99m methoxy isobutyl isonitrile (Tc-99m MIBI) was performed on 12 patients with suspected coronary artery disease at rest and during exercise. Left ventricular wall motion and myocardial perfusion were assessed simultaneously and compared on a segment-by-segment basis. Segmental agreement between Tc-99m MIBI and Tl-201 with regard to the presence of perfusion defects was 95% (57/60) at rest and 93% (37/40) during exercise. With respect to the assessment of myocardial ischemia and/or infarction, abnormalities in regional wall motion agreed with the presence of myocardial perfusion defects in 18 out of 21 segments (86%). Simultaneous evaluation of regional wall motion and myocardial perfusion by Tc-99m MIBI may provide useful information for the assessment of myocardial ischemia.
Adult↗
[Evaluation of non-circular orbit in thallium-201 myocardial SPECT].
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Heart↗
Smooth muscles from spastic coronary artery segments show hypercontractility to histamine.
An animal model of coronary spasm was produced in Göttingen miniature pigs by a selective endothelial denudation of the coronary artery. Five months after the denudation, intracoronary bolus administration of 10 micrograms/kg histamine reduced the luminal diameter angiographically by 57 +/- 16 and 17 +/- 10% (P less than 0.01) in the previously denuded and contralateral control coronary arteries. Muscle fibers of 0.08-0.1 mm wide were prepared from circumferential bundles of the medial smooth muscle in the spastic and nonspastic coronary arteries. Upward shifts of either dose-tonic contraction relationships in Ca2(+)-containing solution or dose-monophasic contraction relationships in Ca2(+)-free solution were noted in muscle fibers taken from the spastic site compared with those from the nonspastic site with no difference between the mean effective dose values. After skinning the muscle fibers with saponin, there was no significant difference in the Ca2+ concentration-tension relationships between the two fibers. These findings suggest that an increased number of histaminergic receptors and/or augmentation of signal transduction, but not Ca2+ sensitivity of the contractile proteins in the medial smooth muscle cells, cause histamine-induced coronary hypercontraction.
Animals↗