Kazuzo Kato

Noninvasive assessment of left and right ventricular filling in myocardial infarction with a two-dimensional Doppler echocardiography method

Inflow characteristics of left and right ventricular filling were assessed in 40 patients with myocardial infarction and in 10 normal subjects by pulsed Doppler echocardiography. Patients with myocardial infarction were subdivided into four groups, focusing on the involvement of right ventricular and septal branches of the coronary arteries. Group I consisted of 11 patients with anterior infarction who showed an obstructive lesion of the proximal left anterior descending branch involving the first septal perforator with a patent right coronary artery. Group II consisted of 10 patients with inferior infarction who showed an obstructive lesion of the proximal right coronary artery involving the right ventricular branch. Group III consisted of 12 patients with both anterior and inferior infarction who showed obstructive lesions of both the proximal left anterior descending branch and the right coronary artery involving the right ventricular branch. Group IV consisted of seven patients with lateral infarction who showed an obstructive lesion of the diagonal branch or branches of the circumflex coronary artery with a patent left anterior descending branch and right coronary artery. Three measurements were performed from the transmitral and transtricuspidal inflow velocity patterns to assess the left and right ventricular diastolic behaviors. These measurements were: acceleration half-time, deceleration half-time of early diastolic rapid inflow, and the ratio of the peak velocity of early diastolic rapid inflow to that of the late diastolic inflow due to the atrial contraction. Impaired diastolic filling of the left ventricle compensated by enhanced left atrial contraction was observed in patients with myocardial infarction from groups I, II, III and IV.(ABSTRACT TRUNCATED AT 250 WORDS)

End-tidal CO2 pressure decreases during exercise in cardiac patients: association with severity of heart failure and cardiac output reserve.

OBJECTIVES We measured end-tidal CO2 pressure (PETCO2) during exercise and investigated the relationship between PETCO2 and exercise capacity, ventilatory parameters and cardiac output to determine the mechanism(s) of changes in this parameter. BACKGROUND It is unclear whether PETCO2 is abnormal at rest and during exercise in cardiac patients. METHODS Cardiac patients (n = 112) and normal individuals (n = 29) performed exercise tests with breath-by-breath gas analysis, and measurement of cardiac output and arterial blood gases. RESULTS PETCO2 was lower in patients than in normal subjects at rest and decreased as the New York Heart Association class increased, whereas the partial pressure of arterial CO2 did not differ among groups. Although PETCO2 increased during exercise in patients, it remained lower than in normal subjects. PETCO2 in relation to cardiac output was similar in patients and normal subjects. PETCO2 at the respiratory compensation point was positively correlated with the O2 uptake (r = 0.583, p < 0.0001) and the cardiac index at peak exercise (r = 0.582, p < 0.0001), and was negatively correlated with the ratio of physiological dead space to the tidal volume. The sensitivity and specificity of PETCO2 to predict an inadequate cardiac output were 76.6% and 75%, respectively, when PETCO2 at respiratory compensation point and a cardiac index at peak exercise that were less than the respective control mean-2 SD values were considered to be abnormal. CONCLUSIONS PETCO2 was below normal in cardiac patients at rest and during exercise. PETCO2 was correlated with exercise capacity and cardiac output during exercise, and the sensitivity and specificity of PETCO2 regarding decreased cardiac output were good. PETCO2 may be a new ventilatory abnormality marker that reflects impaired cardiac output response to exercise in cardiac patients diagnosed with heart failure.

Histological evaluation of coronary plaque in patients with variant angina: relationship between vasospasm and neointimal hyperplasia in primary coronary lesions

OBJECTIVES This study was designed to determine whether coronary vasospasm in patients with variant angina pectoris (VAP) may produce focal organic lesions at the site of vasospasm that would contribute to disease progression. BACKGROUND Recent clinical angiographic and experimental studies have demonstrated the potential role of vasospasm in the worsening of organic coronary stenosis. METHODS We studied histologically the coronary plaques obtained at atherectomy in 202 patients with moderate to severe coronary stenosis. This population included 22 patients with VAP, 100 patients with chronic stable angina and 80 patients with restenosis following angioplasty or atherectomy. Diagnosis of VAP was based on both the clinical feature of angina at rest associated with ST elevation and a positive response to acetylcholine provocation test. RESULTS The most common histological appearance in 92% of patients with stable angina was hypocellular fibroatheromatous plaques, whereas neointimal hyperplasia was the characteristic feature of the plaque observed in 90% of patients with restenosis. The coronary specimens at the site of spasm in 15 of the 22 patients (68%) with VAP demonstrated intimal injuries such as neointimal hyperplasia (15), thrombus formation (2), and intimal hemorrhage (3). Neointimal hyperplasia was significantly more common in the patients with VAP as compared with those with stable angina (68% vs. 8%; p < 0.0001). A rapid progression of organic stenosis within three years was angiographically found in 5 of the 22 patients with variant angina. In all five cases, neointimal hyperplasia was the main contributor to the worsening of the organic lesion at the site of spasm. These histological findings in patients with VAP extremely resembled those in restenosis. Except for vasospasm, no factors significantly predicted the presence of neointimal formations in primary coronary lesions. CONCLUSIONS Coronary vasospasm may provoke vascular injury that leads to the formation of neointima in VAP patients similar to that seen with restenosis. Coronary spasm may thus play a key role in the rapid coronary stenosis progression in certain patients with VAP.

Three dimensional reconstruction of the left ventricle from multiple cross sectional echocardiograms. Value for measuring left ventricular volume.

The accuracy of a system for reconstructing a three dimensional image of the left ventricle from randomly recorded multiple short axis images was tested by comparing the calculated left ventricular volume with the directly measured left ventricular volume in 11 excised porcine hearts. The system comprised a real time phased array sector scanner, a transducer locating system, and a computer system for digitising outlines of the left ventricle, displaying the reconstruction image, and calculating the left ventricular volume. The reconstructed image was similar to the real image and the calculated left ventricular volume showed a high correlation with the directly measured left ventricular volume. This method was accurate in vitro and is expected to be available for clinical measurement of left ventricular volume.

M-mode and cross-sectional echocardiographic study of the left ventricular wall motions in complete left bundle-branch block.

M-mode and cross-sectional echocardiograms of 37 patients with complete left bundle-branch block were compared with those of 5 patients with complete atrioventricular block during right ventricular pacing, 20 patients with anteroseptal infarction, and 20 normal subjects. Of 37 patients with complete left bundle-branch block, 35 showed 3 types (A, B, and C) ofabnormal septal motion and 2 patients showed normal septal motion. In type A and B, early and abrupt posteriorlydirected motion of the septum occurred during the pre-ejection period. After this early abnormal motion, the septum moved anteriorly in type A and posteriorly in type B. Type C exhibited akinetic

Effects of nicorandil on coronary circulation in patients with ischemic heart disease: comparison with nitroglycerin.

In cases where fixed stenosis of coronary arteries plays a predominant role in the pathogenesis of angina pectoris, antianginal drugs can be expected to produce therapeutic effects. By decreasing myocardial oxygen consumption, these drugs improve or even reestablish the normal balance between the myocardial demand for oxygen and the supply of oxygen to myocardial tissues. On the other hand, there is another conceptually important pathophysiologic mechanism of causation of angina pectoris, i.e., dynamic coronary obstruction. Where such a lesion underlies a clinical disease, dilatation of large coronary arteries and relief of coronary spasm account for the main mechanism of action of antianginal drugs. In the present study, the acute coronary hemodynamic and vasodilating effects of nicorandil, a newly developed antianginal drug, were assessed in comparison with nitroglycerin in two groups of ischemic heart disease patients: those with and those without coronary spasm. The results indicate that nicorandil decreased both preload and afterload, though to a lesser extent than nitroglycerin, and also, in striking contrast to nitroglycerin, reduced coronary vascular resistance. The vasodilatory action of nicorandil on the epicardial coronary artery was especially pronounced in cases with increased coronary vascular tonus. Furthermore, the drug strongly potentiated on spontaneous coronary spasm. Nicorandil was thus considered to produce its antianginal effect primarily by redistribution of coronary blood flow as a result of dilatation of vascular beds and by its antispasmodic action.

Effect of Nicorandil on Coronary Spasm

In patients in whom dynamic coronary obstruction plays a predominant role in the pathogenesis of angina pectoris, dilatation of large coronary arteries and relief of coronary spasm account for the main mechanism of action of antianginal drugs. In this study, the acute vasodilating effects of nicorandil, a newly developed antianginal drug, were assessed in 10 patients who had spontaneous and ergonovine-evoked coronary spasms. The prompt, complete relief of both spontaneous and evoked coronary spasms was obtained in all of 10 patients with nicorandil. The coronary spasmolytic effect of nicorandil in the present series is thus considered to be beneficial to the treatment of coronary spasm.

Computer analysis of cross sectional echocardiogram for quantitative evaluation of left ventricular asynergy in myocardial infarction.

Left ventricular asynergy in myocardial infarction was assessed quantitatively by computer analysis of the cross sectional echocardiogram. Short axis cross sectional images of the left ventricle at the levels of the mitral valve, papillary muscle, and apex were recorded by a phased array sector scanner in 30 patients with healed myocardial infarction and 15 normal controls. Endocardial and epicardial short axis images of the left ventricle were transferred from video tape to a minicomputer through the interface circuits, then digitised and processed automatically by a minicomputer. Automatic edge detection of the endocardial and epicardial wall was performed by applying sequential steps including smoothing, second derivative technique, dynamic thresholding, and approximation of boundaries by a spline curve. To quantify regional wall motion, the short axis cross sectional left ventricular wall of each level was divided into eight octants with eight axes at 45 degrees angles from the initial standard axis which was constructed from the geometric centre of the end diastolic left ventricular cavity to the posterior end of the right side of the interventricular septum. Segmental hemiaxis, segmental area, segmental wall thickness, and those changes during cardiac cycle were measured and calculated in each segment automatically by a computer. Regional contractility of the left ventricle was evaluated by percentage systolic changes of the segmental hemiaxis, area, and wall thickness. These values were significantly reduced in the infarcted left ventricular wall as defined by left ventriculography and electrocardiography. Moreover, percentage hemiaxis changes obtained by quantitative left ventriculography described by Herman and colleagues correlated well with those using our analytical method of cross sectional echocardiography in the corresponding segments. The geometric centre of the left ventricular cavity determined by the computer moved slightly towards the anterior wall during systole in normal subjects, possibly reflecting the anterior swinging motion of the heart. The geometric centre of the left ventricular cavity in myocardial infarction moved towards the infarcted wall, showing that the floating reference system was inferior to the fixed reference system for the quantification of abnormal wall motion in myocardial infarction. In conclusion, a computer analysis of the short axis cross sectional echocardiogram of the left ventricle using the fixed reference system has shown its ability to evaluate left ventricular contraction abnormalities, especially systolic wall thickening, which is relatively free of arbitrary interpretation of the wall motion caused by the anterior swinging motion of the heart.

Clinical Efficacy and Safety of Pimobendan in Treatment of Heart Failure – Experience in Japan

The results of Japanese studies on the clinical efficacy and safety of pimobendan in the treatment of heart failure are summarized in this paper. In patients with acute heart failure, a single oral 2.5 mg dose of pimobendan produced a significant increase in cardiac index (27.9%) and stroke volume index (24.4%), as well as a significant decrease in pulmonary capillary wedge pressure (-21.3%). A single oral 5.0 mg dose of pimobendan increased anaerobic threshold during exercise (7.3%). In a multicentre, placebo-controlled, double-blind trial, 8 weeks of treatment with pimobendan 2.5 mg b.i.d., which was suggested to be the optimal dose in a preceding dose-finding study, definitely improved symptoms and signs of heart failure in 52.6% of patients, and New York Heart Association function class in 64.1% of patients. This regimen was also associated with a significantly greater increase in physical activity than placebo. Furthermore, another double-blind, placebo-controlled study suggested that pimobendan 1.25 mg and 2.5 mg b.i.d. may have long-term beneficial effects on morbidity and quality of life in patients with chronic heart failure. Adverse reactions developed in 26 of 241 (10.8%) patients receiving multiple doses of pimobendan, but none of the reactions were serious. It is concluded that pimobendan may be useful in the treatment of patients with heart failure.

Acute effects of intravenous nicorandil on hemodynamics in patients hospitalized with acute decompensated heart failure

BACKGROUND Nicorandil injection, a potent vasodilator with K(ATP) channel opening action and nitrate-like action, has been used for treatment of unstable angina. In the present investigation, we examined the effect of intravenous nicorandil on hemodynamics in patients with acute decompensated heart failure (ADHF). METHODS ADHF patients admitted to hospital with pulmonary artery wedge pressure (PAWP)≥18 mm Hg were enrolled. Patients received nicorandil by an intravenous bolus injection of 0.2mg/kg/5 min followed by continuous infusion at a rate of 0.05, 0.10, or 0.20mg/kg/h for 6h. RESULTS Nicorandil administration caused a significant decrease in PAWP and increase in the cardiac index (CI) that began immediately after the injection and were maintained during the continuous infusion. After 6h, nicorandil administration at 0.2mg/kg/5 min followed by 0.20mg/kg/h resulted in a decrease in PAWP (26.5%, p<0.01), an increase in CI (15.8%, p<0.05), and a decrease in total peripheral resistance (13.8%, p<0.01) in a dose-dependent manner. Nicorandil decreased blood pressure significantly, without an excessive decrease or negative impact even in patients with lower systolic blood pressure. CONCLUSION Intravenous administration of nicorandil, by bolus injection followed by continuous infusion, improves PAWP and CI in ADHF patients immediately and continuously as a potent vasodilator with combined preload and afterload reduction. These results demonstrate that nicorandil is a safe and effective new medication for the treatment of ADHF.