Rinji Murakami

Relationship Between Progressive Microvascular Damage and Intramyocardial Hemorrhage in Patients With Reperfused Anterior Myocardial Infarction Myocardial Contrast Echocardiographic Study

BACKGROUND Recent studies indicated that ischemic microvascular damage may be reversible or progressive after coronary reflow. Intramyocardial hemorrhage is a phenomenon that reflects severe microvascular injury. We examined the relationship between temporal changes in microvascular perfusion patterns detected by myocardial contrast echocardiography (MCE) and intramyocardial hemorrhage detected by magnetic resonance imaging (MRI) in patients with acute myocardial infarction (AMI). METHODS AND RESULTS The study population consisted of 24 patients with anterior AMI. All patients underwent MCE shortly after reflow and in the chronic stage (a mean of 31 days after reflow). Wall motion score (WMS) was determined as the sum of 16 segmental scores (dyskinetic/akinetic=3 to normal=0) at days 1 and 31. Gradient-echo acquisition and gadolinium-DTPA-enhanced spin-echo MRI were performed within 10 days after reflow. In MCE shortly after reflow, 16 patients (67%) showed contrast enhancement and the other 8 patients (33%) showed a sizable contrast defect. In the chronic stage, a persistent contrast defect was observed in 7 of 8 patients with a contrast defect shortly after reflow. Consistent contrast enhancement was observed in 12 of 16 patients (75%) with contrast enhancement shortly after reflow, indicating that a contrast defect newly appeared in 4 patients (25%). Intramyocardial hemorrhage was detected in 9 patients (38%): 5 of 7 patients with a persistent contrast defect and in all 4 patients with a new appearance of a contrast defect during the chronic stage. The patients without hemorrhage showed a significant improvement in WMS compared with patients with hemorrhage at day 31 (5+/-5 versus 19+/-6, P<.0005). CONCLUSIONS These results suggest that irreversible microvascular damage to the ischemic myocardium may cause intramyocardial hemorrhage after reflow, associated with impaired recovery of left ventricular function. Contrast enhancement within the risk area shortly after reflow does not necessarily indicate long-term microvascular salvage.

Hemorrhagic Myocardial Infarction After Coronary Reperfusion Detected In Vivo by Magnetic Resonance Imaging in Humans: Prevalence and Clinical Implications

With the advent of thrombolytic therapy, hemorrhagic myocardial infarction (HMI) has been observed in experimental and human autopsy studies. However, its clinical implications remain undetermined, because of the absence of a reliable method to detect its presence in vivo. This study was designed to evaluate the clinical implications of HMI detected by magnetic resonance (MR) imaging in vivo after coronary reperfusion. Thirty-nine patients with acute myocardial infarction (AMI) were studied. Percutaneous transluminal coronary angioplasty (PTCA) was used to reopen the occluded coronary artery. Electrocardiogram (ECG)-gated T2*-weighted gradient-echo MR imaging was performed to detect intramyocardial hemorrhage, using a 1.5-T magnet within 2 weeks after coronary reperfusion (average, 5.7 days). Thirteen patients (33%) showed intramyocardial hemorrhage as a distinct hypointense zone by gradient-echo MR imaging and 26 patients showed homogeneous intensity consistent with absence of intramyocardial hemorrhage. Coronary angiograms showed lesser development of collateral flow in the patients with HMI than in those without (81% vs. 37%). Infarct size, estimated 1 month after coronary reperfusion by thallium-201 scintigraphy, was larger among patients with HMI than in those without (37 +/- 14% vs. 21 +/- 14%, respectively, p < 0.05). Left ventricular ejection fraction at 1 month follow-up showed less recovery in patients with HMI than in those without (47 +/- 9 to 51 +/- 10%; p = 0.47, vs. 53 +/- 10 to 60 +/- 9%, respectively, p < 0.05). ECG-gated T2*-weighted gradient-echo MR imaging offers a noninvasive means of detection of intramyocardial hemorrhage in patients with reperfused AMI. HMI occurred even after primary PTCA and may be a common finding associated with severely injured myocardium.

Effects of intracoronary infusion of an inotropic agent, E-1020 (loprinone hydrochloride), on cardiac function: evaluation of left ventricular contractile performance using the end-systolic pressure-volume relationship

The phosphodiesterase (PDE) III inhibitor, E-1020 (loprinone hydrochloride), has positive inotropic and vasodilating effects. This study evaluated the positive inotropic effect of intracoronary E-1020 in eight patients with coronary artery disease and hypertensive heart disease. A direct intracoronary infusion of the PDE III inhibitor minimizes its vasodilating effect. After baseline hemodynamic measurements and coronary arteriography, a micromanometer-tipped 8F conductance catheter was introduced into the left ventricle to determine the hemodynamic effects of E-1020. Saline and vehicle were infused into the left main coronary artery at a rate of 2 ml/min. The dose of intracoronary E-1020 increased from 2.5 to 5.0 and 7.5 micrograms/min. The inotropic effect of E-1020 was defined as the change in the slope of the end-systolic pressure-volume relationship (Emax), which was independent of afterload and preload. Emax significantly increased at infusion rates of 7.5 micrograms/min from control. Peak +dP/dt increased at an infusion rate of 5.0 micrograms/min or higher, while left-ventricular end-diastolic pressure (LVEDP) decreased significantly at a rate of 5.0 and 7.5 micrograms/min. Intracoronary infusion of E-1020 at a rate of 2.5 micrograms/min produced a plasma concentration of 20 ng/ml, which was identical to the minimum effective plasma concentration seen in previous study by intra venous infusion. However, at a plasma concentration of 20 ng/ml, E-1020 has more vasodilating effects than inotropic effects. Clinically, E-1020 appears to have a positive inotropic effect that depends on the extent of myocardial perfusion.

Effect of left and right lateral decubitus positions on mitral flow pattern by Doppler echocardiography in congestive heart failure

Abstract In patients with congestive heart failure (CHF), dyspnea is a clinical manifestation of pulmonary venous and capillary hypertension. Patients with CHF usually have 1 type of dyspnea that is limited to 1 lateral decubitus position: trepopnea. 1 In general, patients prefer lying on the right lateral to lying on the left lateral decubitus position. Doppler echocardiographic assessment of the mitral flow provides a considerable amount of information regarding the diastolic filling characteristics of the left ventricle. Mitral flow velocity is mainly determined by the pressure gradient between the left atrium and ventricle, and therefore can be considered to represent the driving force across the mitral valve. 2–4 Previous observations suggested that peak early filling velocity is mainly dependent on the initial driving pressure across the mitral valve. 5,6 Several investigators have shown that increased left atrial pressure increases the early diastolic mitral pressure gradient and peak mitral flow velocity in early diastole, resembling the normal pattern (“pseudonormalization”). 7–9 Little attention is given to the effects of positions on Doppler-derived mitral flow velocities. This study examines the effects of the left and right lateral decubitus positions on Doppler-derived mitral flow velocities in patients with CHF.

Phasic Right Coronary Blood Flow in a Patient with Right Ventricular Hypertension Using Transesophageal Doppler Echocardiography

Although phasic right coronary artery blood flow in right ventricular hypertension has been studied in animals, reports on human subjects are not available. We observed right coronary artery blood flow before and after operation in a patient with right ventricular hypertension secondary to atrial septal defect using transesophageal Doppler echocardiography. Prior to surgery, blood flow was predominantly diastolic in both right and left coronary arteries. Reversal of right ventricular hypertension after surgery resulted in a change in the pattern of right coronary flow, with doubling of flow during systole.

Superior Vena Cava Flow and Tricuspid Anular Motion After Cardioversion of Atrial Fibrillation, and Role of Right Atrial Relaxation on Systolic Venous Return

To determine whether atrial relaxation or systolic descent of the tricuspid anulus is the predominant factor determining systolic venous return, 22 patients with atrial fibrillation were studied. Venous return (i.e., superior vena cava (SVC) flow) was measured using pulsed Doppler echocardiography. Systolic descent of the tricuspid anulus (i.e., total excursion of tricuspid anulus during systole) was also measured using echocardiography. Serial examinations were performed before and after cardioversion of atrial fibrillation in 15 patients. In 11 patients, both the total excursion of the tricuspid anulus and SVC flow were examined in relation to the ratio of the preceding to the pre-preceding RR interval (R2/R1). Systolic forward flow of SVC increased as the ratio of late diastolic to total excursion of the tricuspid anulus (i.e., right atrial systolic function) increased. It correlated significantly with the ratio of late diastolic to total excursion of the tricuspid anulus but not with total excursion. Total excursion of the tricuspid anulus correlated significantly with R2/R1, but systolic forward flow of SVC did not. These results indicate that atrial relaxation rather than systolic descent of the tricuspid anulus was the predominant factor determining systolic forward flow in the SVC.

Transcardiac 5-hydroxytryptamine release and impaired coronary endothelial function in patients with vasospastic angina.

1. The present study was designed to test the hypotheses whether platelet degranulation across the coronary bed is detectable during non‐ischaemic periods in patients with vasospastic angina (VSA) and whether the exogenous nitric oxide (NO) donor nitroglycerin (GTN) is able to modify platelet degranulation, reflecting an impaired endothelial production of NO.

Morphological observation by intravascular ultrasound in superior vena cava syndrome after pacemaker implantation

We report a case of superior vena cava (SVC) syndrome that was assessed by intravascular ultrasound (IVUS). A highly echogenic eccentric lesion was demonstrated by IVUS. The use of IVUS also confirmed in vivo that SVC syndrome following pacemaker insertion occurs as a result of intimal thickening of the venous wall.

Relationship between lipids and angiographically defined coronary artery disease in Japanese patients

The relationship between the severity and extent of coronary artery disease (CAD) and the lipid profiles was evaluated in 120 Japanese male patients, who underwent coronary angiography. Analysis of the lipid quartile distribution showed that the percentage of patients with significant CAD increased as the total cholesterol (TC) increased and high-density lipoprotein cholesterol (HDL-C) decreased. In addition, as the number of vessels with marked coronary artery stenosis increased, TC and TC/HDL-C increased while HDL-C decreased. However, within this population, triglyceride level, high blood pressure, and smoking were not significantly associated with coronary angiographic findings.

Comparison of acetylene rebreathing and thermodilution methods for determining cardiac output

The usefulness of the acetylene rebreathing method in the noninvasive determination of cardiac output was compared with that of the thermodilution method. Simultaneous measurements of cardiac output by the acetylene rebreathing method and the thermodilution method were performed at rest in 20 patients with cardiac disease or hypertension and additionally during ergometer exercise in the supine position in 9 of 20 cases