Kenichi Fukami

Intravascular ultrasound evaluation of coronary plaque regression by low density lipoprotein-apheresis in familial hypercholesterolemia: the Low Density Lipoprotein-Apheresis Coronary Morphology and Reserve Trial (LACMART).

OBJECTIVES We sought to assess the effects of low density lipoprotein (LDL)-apheresis (LDL-A) for regression of coronary plaque in familial hypercholesterolemia (FH), we set up a one-year follow-up multicenter trial using coronary angiography and intravascular ultrasound (IVUS). BACKGROUND It is still unclear whether aggressive lipid-lowering therapy by LDL-A leads to the regression of coronary plaque in patients with FH. METHODS Eighteen patients with FH were assigned to one of two groups: medication + LDL-A (LDL-A group, n = 11) and medication only (medication group, n = 7). Total cholesterol, triglycerides, high density lipoprotein cholesterol and LDL cholesterol were measured in all subjects at the outset of treatment (baseline) and every three months thereafter. Coronary angiography and IVUS were performed at the outset and after the one-year follow-up period to measure minimal lumen diameter (MLD) by coronary angiogram and plaque area (PA) by IVUS. RESULTS The LDL-A group showed 28.4% reduction in total cholesterol (from 275 +/- 27 mg/dl to 197 +/- 19 mg/dl) and 34.3% reduction in LDL cholesterol (from 213 +/- 25 mg/dl to 140 +/- 27 mg/dl) after one-year follow-up, while the medication group showed no changes in cholesterol levels. There were significant interactions between both treatments in total cholesterol (p = 0.0001), LDL cholesterol (p = 0.0001), MLD (p = 0.008) and PA (p = 0.017) using two-way repeated-measures analysis of variance by the SAS system (SAS Institute Inc., Cary, North Carolina). Significant differences were seen in net change in MLD (p = 0.004) and PA (p = 0.008) during the one-year follow-up period between both groups. CONCLUSIONS These results suggest that aggressive lipid-lowering therapy using the combination of LDL-A and lipid-lowering drugs may induce regression of coronary atherosclerotic plaque in FH patients.

Long-term prognosis of patients with acute myocardial infarction: Is mortality and mortidity as low as the incidence of ischemic heart disease in Japan?

Long-term prognosis of hospital survivors with myocardial infarction (MI) was investigated to assess the validity of previous reports on the low incidence of ischemic heart disease in Japan. Among 686 patients with acute MI, 115 (16.8%) died during hospitalization and eight were lost to follow-up. The cumulative mortality rate of the 563 hospital survivors was 6.2% in the first year, 12.0% in the third year, and 19.1% in the fifth year, with cardiac death accounting for 63% of the deaths. Cumulative rates for recurrent MI were 4.4% in the first year, 11.0% in the third year, and 13.2% in the fifth year. Parameters influencing long-term mortality rates obtained by stepwise discriminant analysis were arteriosclerosis-related factors, presence of congestive heart failure at admission, age, and presence of previous MI, while parameters influencing the recurrence of MI were congestive heart failure, arteriosclerosis-related factors, and ischemic findings at discharge. Our findings indicate that the prognosis for patients with MI is far better in Japan than in Western countries and support the previous reports on the low incidence of ischemic heart disease in Japan, while factors influencing the prognosis are similar to those previously reported.

Comparison of clinical features of non-Q wave and Q wave myocardial infarction

The clinical spectrum and outcome of 119 patients with acute non-Q wave myocardial infarction (NQMI) were studied, in comparison with those of 354 patients with acute Q wave myocardial infarction (QMI). The patients with NQMI had a significantly higher incidence of preinfarction angina (73% vs 63%), previous myocardial infarction (43% vs 22%), multivessel disease (73% vs 51%), postinfarction angina (55% vs 21%), and recurrent myocardial infarction during follow-up for an average of 25 months (17% vs 8%). NQMI patients also had a lower rate of complication of pump failure and smaller infarct size estimated by peak creating phosphokinase (CPK) levels (1361 +/- 1243 vs 2711 +/- 1684 IU/L) than those with QMI. There was no difference in in-hospital mortality between the two groups (17% vs 17%). However, death due to cardiac rupture was exclusively noted in the QMI group. The present study suggests that NQMI is more unstable than QMI in the clinical course.

Effects of right ventricular ischemia on left ventricular geometry and the end-diastolic pressure-volume relationship in the dog.

We studied the effects of right ventricular ischemia on left ventricular three-dimensional geometry and the end-diastolic pressure-volume relationship in 16 open-chest dogs before and after pericardiectomy. Left ventricular volume was calculated from three internal dimensions measured with ultrasonic crystals. In one group of eight dogs, right coronary artery (RCA) occlusion for 2 min with the pericardium intact reduced aortic flow by 24 +/- 9% (p less than .001) and septal-lateral dimension by 8 +/- 5% (p less than .01), without changing anterior-posterior and apical-basal dimensions. However, parameters of left ventricular systolic function (aortic flow, left ventricular systolic pressure, peak dP/dt, and mean percent systolic shortening) were similar to those observed at a comparable level of left ventricular end-diastolic volume during inferior vena caval occlusion. In the other group of eight dogs, during RCA occlusion before pericardiectomy the left ventricular end-diastolic pressure-volume relationship determined during rapid blood transfusion shifted leftward and upward significantly from the preocclusion relationship. After pericardiectomy, RCA occlusion caused less significant changes in aortic flow and septal-lateral dimension as well as in the left ventricular end-diastolic pressure-volume relationship. We concluded that right ventricular ischemia causes a leftward shift of the interventricular septum in end-diastole and an alteration of the left ventricular end-diastolic pressure-volume relationship without changing left ventricular myocardial performance. These changes are enhanced by the intact pericardium.

Classification of non-Q-wave myocardial infarction according to electrocardiographic changes.

The characteristics of 93 patients in whom electrocardiographic recordings were obtained within 12 hours of the onset of non-Q-wave myocardial infarction were studied. Patients were divided into the three groups according to what electrocardiographic changes were seen. Forty nine patients had ST segment depression, 35 had ST segment elevation, and nine had T wave changes. Patients with ST segment depression had a higher rate of pump failure and multivessel disease than the other two groups. There were no significant differences in peak serum creatine kinase activity among the three groups. Twelve of 13 patients who died of non-Q-wave myocardial infarction in hospital had ST segment depression. Furthermore nine of them had attacks of non-Q-wave myocardial infarction with severe ST segment depression in many leads. At necropsy five of six patients who had shown severe ST segment depressions in many leads at the onset of non-Q-wave myocardial infarction were found to have circumferential subendocardial lesions with triple vessel disease. This study suggests there are electrocardiographic subtypes of non-Q-wave myocardial infarction that are associated with specific patient characteristics.

Transient Cortical Blindness Following Bypass Graft Angiography A Case Report

Transient cortical blindness, an uncommonly recognized complication of cerebral angiog raphy, is an exceedingly rare event after cardiac catheterization and angiography. This report describes a sixty-two-year-old patient who had transient cortical blindness following bypass graft angiography. In this case, the authors showed that cortical blindness was associated with the breakage of the blood-brain barrier (BBB) and an increase in vascular permeability rather than with primary cerebral circulatory insuffi ciency. When the possibility exists that an excess volume of contrast medium may enter the cerebral circulation as in this case, that is, following a coronary artery bypass graft (CABG) using the internal mammary artery (IMA), precautionary measures may be necessary such as changing the type of contrast medium to be used or decreasing the volume injected. When cortical blindness occurs, it is a serious clinical problem whether transient or permanent. Therefore, the circumstances leading to this complication should be understood to determine suitable treatment and management.

Noninvasive Measurement of Left Coronary Blood Flow Reserve by Transthoracic Doppler Echocardiography: Comparison with Doppler Guidewire Ultrasonography.

The development of new ultrasound instrumentation has made epicardial coronary artery blood flow imaging easier with the use of transthoracic coronary Doppler echocardiography (TCDE). This study was performed to investigate the accuracy of coronary blood flow reserve (CFR) measurement by TCDE. In 15 patients with ischemic heart disease in the absence of valvular disease or atrial fibrillation, coronary flow at rest and flow with hyperemia induced by intravenous dipyridamole infusion were recorded by TCDE and Doppler guidewire ultrasonography. The CFR was determined as the ratio of the maximum hyperemic diastolic time‐averaged peak velocity to the velocity at rest in the proximal or distal left anterior descending coronary artery. It was found that the CFR of the left anterior descending coronary artery measured by TCDE was comparable in accuracy with CFR measured by invasive methods (r = 0.87, P < 0.0001, n = 15).

Survival Following Cardiogenic Shock Caused by Acute Left Main Coronary Artery Total Occlusion A Case Report and Review of the Literature

The authors describe a fifty-five-year-old Japanese man with an acute extensive anterior myocardial infarction associated with a total occlusion of the left main coronary artery. The patient suffered cardiogenic shock and was treated successfully with rescue percu taneous transluminal coronary angioplasty and an intraaortic balloon pump (IABP) after unsuccessful intracoronary thrombolysis. Ten days after admission, he was weaned from IABP, and recovery-phase coronary angiography revealed no significant coronary artery stenosis and an ejection fraction of 32% by left ventriculography. The patient was discharged from the hospital without any ischemic findings.

A case of variant angina exacerbated by administration of rifampicin

SummaryRifampicin, an antituberculosis agent, is known to be a potent inducer of microsomal drug-metabolizing enzymes in the liver. Elimination or clearance of many drugs has been reported to be enhanced, and their effectiveness reduced; however, no report in the literature has dealt with the interaction between rifampicin and dihydropiridine calcium entry-blocking drugs such as nifedipine. We present here evidence for the possible interaction between rifampicin and nifedipine in a patient with angina pectoris, which was exacerbated during coadministration or rechallenge with rifampicin. The peak plasma level and area under the curve were reduced and the apparent oral clearance of nifedipine was increased by rifampicin, suggesting that rifampicin enhanced the elimination of nifedipine via induction of a hepatic microsomal drug-metabolizing enzyme, as has been reported on other drugs widely metabolized in the liver.

Clinical Application of Ischemic Preconditioning by ATP-Sensitive Potassium Channel Openers

Prognosis after myocardial infarction is dependent on infarct size, which reflects left ventricular dysfunction. It is therefore important to explore a strategy for reducing infarct size in patients with acute myocardial infarction. It has been reported that infarct size derived from regional wall motion of the left ventricle or calculated from total release of cardiac enzymes and the rate of incidence of cardiogenic shock after acute myocardial infarction was significantly decreased in patients with a history of angina pectoris compared to those without pre-infarction angina.1