Hiroya Taniguchi

Atrial fibrillation in inferior wall Q-wave acute myocardial infarction.

Abstract Although atrial fibrillation (AF) is a relatively common arrhythmia occurring during the course of acute myocardial infarction (AMI), the mechanisms involved in its genesis remain controversial and are mostly focused on the left ventricle and atrium: left ventricular failure, pericarditis and left atrial ischemia.1–4 In contrast, the role of hemodynamic change imposed on the right ventricle and right atrium related to the onset of AF after AMI is poorly understood. Because hemodynamic change of the right ventricle is often observed in inferior AMI, we hypothesized that hemodynamic impairment, audible pericardial friction rub, electrocardiographic evidence of right ventricular AMI and age may be important clinical factors associated with the occurrence of AF. In this study, multivariate analysis was used to assess the clinical settings associated with the occurrence of AF in patients with their first Q-wave inferior AMI.

Mixed venous oxygen saturation as a guide to tissue oxygenation and prognosis in patients with acute myocardial infarction

The relation of mixed venous oxygen saturation and the cardiac index to tissue oxygenation and prognosis was investigated in 119 patients with acute myocardial infarction. There was a positive correlation between mixed venous oxygen saturation and the cardiac index in 97 survivors and 22 nonsurvivors, but a significantly lower mixed venous oxygen saturation level at the same level of cardiac index was observed in nonsurvivors compared with survivors. Results of multivariate analysis with mixed venous oxygen saturation and the cardiac index indicated that only mixed venous oxygen saturation was significantly related to survival and to hyperlactacidemia. Oxygen delivery to tissues declined significantly in nonsurvivors because of a lower cardiac index and a lower hemoglobin concentration in these patients than in survivors. However, at the same level of oxygen delivery to tissues, nonsurvivors had a significantly higher rate of oxygen consumption leading to a correspondingly greater decrease in mixed venous oxygen saturation, suggesting that a greater increase in oxygen demand was also observed in nonsurvivors than in survivors. Thus mixed venous oxygen saturation after acute myocardial infarction is a better predictor of hyperlactacidemia and survival than the cardiac index, and this may be associated with an increased oxygen demand and an impaired oxygen transport system in seriously ill patients.

INCREASED EXTRAVASCULAR LUNG WATER IN PATIENTS WITH LOW PULMONARY ARTERY OCCLUSION PRESSURE AFTER ACUTE MYOCARDIAL INFARCTION

ObjectiveTo evaluate the clinical characteristics of increased extravascular lung water (EVLW) in patients with low pulmonary artery occlusion pressure (PAOP) in the early phase of acute myocardial infarction. DesignConsecutive sample for descriptions of the clinical features of medical disorders. SettingA general medicine group practice in a university hospital. PatientsSixteen patients with low PAOP (>18 mm Hg) on the initial measurement obtained within 12 hr of chest pain onset. Measurements and Main ResultsEVLW was measured by the thermal indocyanine green dye double-indicator dilution method. QRS score was obtained on hospital day 7 from the Selvesters QRS Scoring System. Eleven (69%) patients had increased EVLW >7 mL/kg despite low PAOP. EVLW had no significant correlation with PAOP and the difference between plasma colloid osmotic pressure and PAOP, but did have a significant correlation with pulmonary vascular resistance index (r2 = .31, p < .05), and QRS score (r2 = .45, p < .005). ConclusionLarger infarcts led to increased EVLW even with low PAOP, and the accumulation of increased EVLW around the small arterioles might have led to increased pulmonary vascular resistance. (Crit Care Med 1991; 19:21)

Acute pulmonary edema in patients with unstable angina: clinical profile and natural history

BackgroundPulmonary edema is an important manifestation of ischemic cardiac dysfunction, both in the presence and absence of myocardial infarction. However, the clinical characteristics and natural history of pulmonary edema with unstable angina have not been fully evaluated. MethodsOne hundred twenty patients admitted to our hospital within 6 hours from the onset of last chest pain were studied. Clinical features were reviewed from hospital charts and coronary angiography was performed in acute phase (33 patients) and in the late hospital phase (62 patients). The mean follow-up period was 26 months. Results: Pulmonary edema was present in 24 patients and was absent in 96 patients. The duration of chest pain was longer (P<0.01) and incidence of multivessel disease was higher (P<0.01) in patients with pulmonary edema than those without it. The total mortality rate in patients with pulmonary edema was higher that those without it (33% vs 3%; P<0.001). These data indicate that a large mass of ischemic myocardium could cause transient increase of left ventricular diastolic pressure to pulmonary edema level without infarction ever occurring. ConclusionsBecause of the high incidence of multivessel disease and the poor prognosis in patients with pulmonary edema in unstable angina, early and aggressive diagnostic efforts should be undertaken to exclude viable segments of myocardium in patients with unstable angina complicated by pulmonary edema.

Effect of atrial and ventricular activation interval on hemodynamics during atrioventricular and ventriculoatrial pacing : determination from pressure-volume loops in dogs

To determine the effect of relative timing of atrial and ventricular activation on hemodynamic indices, we evaluated pressure-volume loops during pacing at 160 beats/min with various atrioventricular intervals in dogs. End-systolic pressure, end-diastolic volume, and stroke volume were reduced during pacing at atrioventricular intervals of 0 ms, compared with 80 ms. These changes were more significant during pacing at atrioventricular intervals of -50 and -100 ms than at 0 ms. During tachycardia, the abnormal timing of atrial contraction leads to unfavorable hemodynamic change and the degree of the changes are determined by the ventriculoatrial activation interval.