Comparative effect of clinidipine and quinapril on left ventricular mass in mild essential hypertension.

The aim of this study was to compare the regressive effect of clinidipine on left ventricular mass (LVM) with that of quinapril. Sixty patients with mild essential hypertension aged more than 39 years were randomly allocated to two groups to receive cilnidipine (10 mg; n = 30) or quinapril (10 mg; n = 30). The patients underwent echocardiography before and 12 months after drug treatment. Sixteen patients in each group underwent 123I-metaiodobenzylguanidine (MIBG) cardiac imaging before and 12 months after drug treatment. In both groups systolic and diastolic blood pressures significantly decreased to similar levels. In the clinidipine group, both end-diastolic and end-systolic diameters and posterior wall thickness significantly decreased, while only end-systolic diameter significantly decreased in the quinapril group. However, LVM (206 +/- 36 g to 189 +/- 40 g, p < 0.02 for the quinapril group, 195 +/- 60 g to 171 +/- 48 g, p < 0.004 for the clinidipine group) and the LVM index (127 +/- 20 g/m2, to 116 +/- 20 g/m2, p < 0.02 for the quinapril group, 121 +/- 32 g/m2 to 106 +/- 24 g/m2 p < 0.003 for the clinidipine group) significantly decreased in both groups. Regarding MIBG imaging, in the cilnidipine group, the heart-to-mediastinum ratio significantly increased (p < 0.02) and the washout rate significantly decreased (p < 0.02) after drug treatment. In contrast, there were no significant changes in MIBG parameters in the quinapril group. Clinidipine produced a greater decrease in LVM in essential hypertension than quinapril, probably due to the long-term suppression of the cardiac sympathetic nervous system. Clinidipine is useful for hypertensive patients with left ventricular hypertrophy and may improve their prognosis.

Diffuse and severe left ventricular dysfunction induced by epicardial coronary artery spasm.

Endothelial dysfunction and effectiveness of treatment of calcium antagonists are suggestive of coronary artery spasm as an underlying disorder in dilated cardiomyopathy (DCM). The aim of this study is to determine whether or not the epicardial coronary artery spasm can induce severe cardiac dysfunction like DCM. Thirty-four consecutive patients with angiographically normal coronary arteries and diffuse left ventricular hypokinesis whose causes had been unknown underwent acetylcholine provocation test and left ventricular biopsy. Eight patients were excluded according to the clinical and laboratory data and biopsy findings suggesting myocarditis or other systemic diseases. According to the results of the acetylcholine provocation test, 17 patients were finally diagnosed as having DCM, and nine patients (35% of the study patients), who had acetylcholine-induced diffuse and multivessel coronary spasm, were diagnosed as having DCM-like vasospastic angina pectoris (VSA). Clinical and cardiac catheterization data including hemodynamics and biopsy findings were similar between the two groups except that left ventricular end-systolic volume was significantly greater in DCM than in DCM-like VSA. After the acetylcholine provocation test, DCM patients received both a beta blocker and an angiotensin-converting enzyme inhibitor, and DCM-like VSA patients received antianginal drugs. In echocardiographic findings at predischarge and those after 6-month drug treatment, both DCM-lke VSA and DCM showed significant reduction in end-diastolic and end-systolic diameters and significant increase in fractional shortening and ejection fraction, whereas changes in ejection fraction and fractional shortening were significantly greater in DCM-like VSA than those in DCM. Epicardial coronary artery spasm can induce diffuse and severe left ventricular dysfunction like DCM in VSA. Although antianginal drugs markedly improve left ventricular function of these patients, only the acetylcholine provocation test can identify DCM-like VSA.

Cardiac sympathetic dysfunction contributes to left ventricular remodeling after acute myocardial infarction.

To investigate the role of the cardiac sympathetic nervous system in left ventricular remodelling, 50 patients with first-time acute myocardial infarction (AMI) and patency of the infarct-related artery after reperfusion underwent quantitative iodine-123 metaiodobenzylguanidine (MIBG) imaging at 4 days and 4 weeks (n=42), and quantitative technetium-99m tetrofosmin imaging at 2 days after AMI. They also underwent both ventriculography and coronary angiography on admission and about 4 weeks after AMI. On the basis of left ventricular end-systolic volume (LVESV), patients were divided into two groups. Patients with LVESV dilatation (n=20) had a significantly lower ejection fraction (P<0.003) and a significantly higher severity score of 99mTc-tetrofosmin (P<0.04), and total severity (P<0.01), delta extent (P<0.007) and delta severity (P<0.0008) scores of MIBG than patients without LVESV dilatation (n=30). delta severity score of MIBG was directly correlated with change in LVESV at 4 weeks (r=0.63, P<0.0001). Stepwise linear discriminant function analysis showed that delta severity score of MIBG (P<0.0002) was the only discriminator of LVESV dilatation. Patients with LVESV dilatation had higher regional washout rates in both the infarct and the non-infarct zones than patients without such dilatation. Furthermore, no MIBG parameters changed significantly between 4 days and 4 weeks after AMI. In reperfused AMI, delta severity score of MIBG was related to the degree of ventricular dilatation and was the only powerful discriminator of ventricular dilatation. These results suggest that cardiac sympathetic nervous abnormality might contribute to left ventricular remodelling in reperfused AMI. MIBG imaging may allow identification of reperfused AMI patients at high risk for left ventricular remodelling.

Scintigraphic assessment of regional cardiac sympathetic nervous system in patients with single-vessel coronary artery disease.

In coronary artery disease, the cardiac sympathetic nervous system is closely associated with myocardial ischemia. I-123 metaiodobenzylguanidine (MIBG) imaging allows us to assess the cardiac sympathetic nervous system regionally. One-hundred and eleven patients with single-vessel disease underwent regional quantitative analysis of MIBG imaging before successful percutaneous transluminal coronary angioplasty (PTCA), and repeat angiography 6 months after PTCA. Based on the results of the follow-up left ventriculogram, patients were divided into 3 groups: 39 angina pectoris (AP), 48 prior myocardial infarction without asynergy (MI without asynergy) and 24 prior myocardial infarction with asynergy (MI with asynergy). AP and MI without asynergy had significant correlations between uptake parameters and regional washout in the territory of diseased vessels, among which the severity score in AP was the most closely correlated with regional washout (r = 0.79, p < 0.0001). These correlations disappeared in MI with asynergy. To compare regional MIBG parameters in the territory of the diseased vessel as well as in the territories of the other major coronary arteries among the 3 groups, we examined MIBG parameters in 57 patients with left anterior descending artery (LAD) disease selected from among the study patients. Regional washout in the territory of the LAD was significantly higher in the MI without asynergy group than in the other two groups. The left circumflex artery (LCX) region showed significantly reduced MIBG uptake and an increased extent score in the MI with asynergy group compared with the AP group, although only a difference in the extent score existed between the MI with asynergy group and the AP group in the right coronary artery (RCA) region. In addition, the global ejection fraction before PTCA showed a significant negative correlation with each regional washout rate. In this way, regional quantitative analysis of MIBG imaging can detect the regional differences in the cardiac sympathetic nervous system in coronary artery disease, which may be associated with the degree of regional left ventricular dysfunction due to myocardial ischemia.

Pseudoxanthoma elasticum with dipyridamole-induced coronary artery spasm: a case report.

In patients with pseudoxanthoma elasticum, severe organic coronary artery stenosis often occurs without coronary risk factors. However, this report presents the case of a 49-year-old woman with pseudoxanthoma elasticum who had coronary artery spasm with an angiographically normal coronary artery. In addition, coronary artery spasm was provoked with dipyridamole thallium-201 cardiac imaging.

[Slowly progressive IDDM with rheumatoid arthritis and Hashimoto disease in high elderly].

We report a 79-year-old woman case of slowly progressive IDDM (SPIDDM) with rheumatoid arthritis (RA) and Hashimoto disease. High titer of anti-glutamic acid decarboxylase antibody (GAD) with a value of 16,400 U/ml (normal value: less than 5 U/ml) and deteriorated secretion of insulin, and clinical course led to the diagnosis of SPIDDM. Both anti-islet cell and anti-insulin antibodies were negative. One year prior to the diagnosis, at 78 years of age, she was newly diagnosed with NIDDM and had been medicated with sulfonylurea and voglibose, resulting her glucose levels well-controlled. Four months before admission, a gradual increase of plasma glucose was noticed, while oral hypoglycemic agents were fully administrated. On admission, her glycemic control was revealed as follows; a fasting blood glucose level of 458 mg/dl and an HbA1 C level of 14.3%. Urinary CPR was 22.5 micrograms day. Her insulin secretion was proved not to be induced with intravenous glucagon injection. Hyperinsulinemic euglycemic glucose clamp test showed the normal glucose uptake ratio; 9.5 mg/kg/min. Moderate doses of subcutaneous insulin (20 units daily) were effective on her diabetes control. She was newly diagnosed with Hashimoto disease that required thyroid hormone replacement 50 micrograms per day after having developed NIDDM. High titer of anti-thyroglobulin antibody (46.9 U/ml) and anti-thyroid peroxidase antibody (81.5 U/ml) were observed. The patient had been medicated for RA with anti-inflammatory drugs since her early seventieth. Rheumatoid factor was elevated to 127.7 IU/L and, anti-nuclear antibody (x 80) and anti-DNA antibody (x 80) were present. It may be of interest that a specific phenotype of HLA; A24 (9) and DR9 recognized to be susceptible to IDDM was detected in the high-elderly onset SPIDDM. Taken together HLA typing with her history of both RA and Hashimoto disease, our case may provide the information to the mechanism of pathogenesis of SPIDDM. Furthermore, to out knowledge, this is the first case of SPIDDM in the aged; 75-year-old or more.