Tadafumi Joh

Plasma lipids and lipoproteins in Japanese male patients with coronary artery disease and in their relatives

Plasma cholesterol (CH), triglyceride (TG) and high density lipoprotein cholesterol (HDL-C) were measured in 92 consecutive Japanese male subjects undergoing diagnostic coronary cineangiography. Sixty-nine of them were classified as having coronary artery disease (CAD), the remaining 23 subjects were classified as having normal coronary arteries (NCA). The CAD group had significantly lower HDL-C and higher TG levels than the NCA group. However, there was no significant difference in plasma CH between the two groups. First-degree relatives of the CAD patients were also investigated. The male blood relatives of the CAD patients also had significantly lower HDL-C and higher TG levels than the non-blood male relatives and healthy control males. The female blood relatives, however, showed no significant differences from the non-blood female relatives and the healthy control females in plasma CH, TG and HDL-C levels. These results suggest that low HDL-C and hypertriglyceridemia are the prevalent coronary risk factors, rather than hypercholesterolemia, in a population with a low fat intake such as the Japanese, and that these lipid abnormalities are related to sex and genetic factors.

Both a Calcium Antagonist and ACE Inhibitor Reverse Hypertrophy in Hypertension But a Calcium Antagonist also Depresses Contractility

The aim of this study was to compare the effects of a calcium antagonist, nicardipine SR, with an angiotensin-converting enzyme (ACE) inhibitor, alacepril, on the regression of left ventricular hypertrophy (LVH) and function. Twenty patients with LVH, aged 42–73 years, were treated with nicardipine SR or alacepril. Ten patients were treated with nicardipine SR (40–80 mg) for 21 months, and the other 10 patients were treated with alacepril (25–100 mg) for 18 months. All patients underwent echocardiography to assess left ventricular structure and function before and after the treatment. After nicardipine SR or alacepril treatment, blood pressure was decreased significantly from 176.0 ± 13.9/97.0 ± 5.3 mmHg to 140.0 ± 14.0/77.4 ± 7.2 mmHg and from 168.2 ± 22.3/99.0 ± 5.5 mmHg to 138.4 ± 12.5/85.2 ± 9.7 mmHg, respectively (both p < 0.01), whereas heart rate did not change (73.8 ± 14.6 beats/min vs. 69.9 ± 13.5 beats/min and 71.6 ± 9.7 vs. 65.8 ± 8.1 beats/min, respectively). The left ventricular mass index decreased significantly from 133.2 ± 11.7 g/m2 to 114.4 ± 15.7 g/m2 with nicardipine SR and from 137.1 ± 14.8 g/m2 to 99.3 ± 23.0 g/m2 with alacepril (both p < 0.01). The fractional shortening, peak shortening rate, and peak lengthening rate all improved significantly after each treatment. The end-systolic wall stress/left ventricular end-systolic volume index, as an index of left ventricular contractility, was decreased significantly after treatment with nicardipine SR but was not changed after treatment with alacepril. In conclusion, both nicardipine SR and alacepril similarly reduced LVH and improved left ventricular systolic and diastolic function. However, alacepril did not alter left ventricular contractility, whereas nicardi-pine SR decreased left ventricular contractility.

Effects of Long‐Term Treatment with Sustained‐Release Nicardipine on Left Ventricular Hypertrophy and Function in Patients with Essential Hypertension

The effects of long‐term treatment with sustained‐release nicardipine (nicardipine SR) on left ventricular hypertrophy and junction were studied. Ten uncomplicated essential hypertensive patients with left ventricular hypertrophy, aged 61 ± 7.6 years old, were treated with nicardipine SR alone for an average of 20 months (range: 12–26 months). All patients underwent echocardiography for assessment of left ventricular diameters and function before and after the treatment At the end of the treatment, systolic and diastolic blood pressures significantly decreased from 176.0 ± 13.9 to 140.0 ± 14.3 mm Hg and from 97.0 ± 5.3 to 77.4 ± 7.2 mm Hg, respectively (each P < 0.01), while heart rate did not change (73.6 ± 14.6 vs. 69.9 ± 13.5 beats/min). The left ventricular mass index significantly decreased from 132.1 ± 14.4 to 114.4 ± 15.7 g/m2 (P < 0.01) due to significant reductions in both interventricular septal thickness (P < 0.01) and left ventricular posterior wall thickness (P 0.05). The ejection fraction (EF), fractional shortening (FS), peak shortening rate (PSR), and peak lengthening rate (PLR) were also improved significantly by the treatment (EF and FS, P < 0.05; PSR and PLR, P < 0.01). Significant inverse relationships existed between end‐systolic wall stress and peak shortening or lengthening rate before the treatment (r = 0.80, P < 0.05; r = 0.86, P < 0.05, respectively). These relationships were unchanged after the treatment. Nicardipine SR reduced left ventricular hypertrophy and improved both left ventricular systolic and diastolic functions without causing any consistent augmentation of intrinsic left ventricular function in essential hypertensive patients with left ventricular hypertrophy.

[Effective low-dose amiodarone therapy for ventricular tachycardia complicated with ischemic heart disease and poor left ventricular function in an elderly patient].

A 71-year-old man who had ischemic heart disease with poor left ventricular function and ventricular tachycardia was admitted to hospital for evaluation. Cardiac catheterization was performed on August 19, 1996, and right coronary arteriography revealed total occlusion at segment 3. Left coronary arteriography revealed total occlusion at segment 6, and a lesion at segment 13 was 75% occluded. Partial collateral flow from the right ventricular branch to the left anterior descending artery was demonstrated, and the left ventricular ejection fraction was 24%. Recurrent ventricular tachycardia followed by pre-syncope occurred from August 23, 1996, and the patient underwent emergency coronary artery bypass surgery to the left anterior descending artery and circumflex artery using saphenous vein grafts. Ventricular tachycardia followed by pre-syncope occurred frequently after the bypass surgery, and antiarrhythmic agents (Vaughan Williams classification Ia and Ib groups) were ineffective. He received amiodarone (100 mg/day after a loading dose of 200 mg/day for 2 weeks) from September 6, 1996. His symptoms of arrhythmia decreased, and side effects have not been observed. Low-dose amiodarone was effective in this case of ischemic heart disease with left ventricular dysfunction and sustained ventricular tachycardia.