Significant Correlates of Nocturnal Hypertension in Patients With Hypertension Who Are Treated With Antihypertensive Drugs.

BACKGROUND: Nocturnal hypertension assessed by a home blood pressure monitoring (HBPM) device is associated with an increased risk of cardiovascular events. However, it is still difficult to assess nighttime blood pressure (BP) frequently. The purpose of this cross-sectional study was to identify significant correlates of nocturnal hypertension assessed by an HBPM device in patients with hypertension who are treated with antihypertensive drugs. METHODS: We measured nighttime BP, morning BP, and evening BP by an HBPM device for 7 consecutive days in 365 medicated patients with hypertension. RESULTS: Of the 365 subjects, 138 (37.8%) had nocturnal hypertension defined as a mean nighttime systolic BP of ≥ 120 mm Hg. Receiver operating characteristic curve analyses showed that the diagnostic accuracy of morning systolic BP for subjects with nocturnal hypertension was significantly superior to that of evening systolic BP (P = 0.04) and that of office systolic BP (P < 0.001). Multivariate analysis revealed that morning systolic BP of 125-<135 mm Hg (odds ratio [OR], 2.26; 95% confidence interval [CI], 1.13-4.58; P = 0.02), morning systolic BP of ≥ 135 mm Hg (OR, 16.4; 95% CI, 8.20-32.7; P < 0.001), and a history of cerebrovascular disease (OR, 3.99; 95% CI, 1.75-9.13; P = 0.001) were significantly associated with a higher risk of nocturnal hypertension and that bedtime dosing of antihypertensive drugs was significantly associated with a lower risk of nocturnal hypertension (OR, 0.56; 95% CI, 0.32-0.97; P = 0.04). CONCLUSIONS: Morning systolic BP of ≥ 125 mm Hg, a history of cerebrovascular disease, and bedtime dosing were significant correlates of nocturnal hypertension in medicated patients with hypertension, and may help detect this risky BP condition. CLINICAL TRIALS REGISTRATION: University Hospital Medical Information Network Clinical Trials Registry (UMIN000019173).

Pitfalls in 16-detector row CT of the coronary arteries.

Recently developed 16-detector row computed tomography (CT) has been introduced as a reliable noninvasive imaging modality for evaluating the coronary arteries. In most cases, with appropriate premedication that includes beta-blockers and nitroglycerin, ideal data sets can be acquired from which to obtain excellent-quality coronary CT angiograms, most often with multiplanar reformation, thin-slab maximum intensity projection, and volume rendering. However, various artifacts associated with data creation and reformation, postprocessing methods, and image interpretation can hamper accurate diagnosis. These artifacts can be related to pulsation (nonassessable segments, pseudostenosis) as well as rhythm disorders, respiratory issues, partial volume averaging effect, high-attenuation entities, inappropriate scan pitch, contrast material enhancement, and patient body habitus. Some artifacts have already been resolved with technical advances, whereas others represent partially inherent limitations of coronary CT angiography. Familiarity with the pitfalls of coronary angiography with 16-detector row CT, coupled with the knowledge of both the normal anatomy and anatomic variants of the coronary arteries, can almost always help radiologists avoid interpretive errors in the diagnosis of coronary artery stenosis.

Influence of angiotensinogen M253T gene polymorphism and an angiotensin converting enzyme inhibitor on restenosis after percutaneous coronary intervention.

We studied the relation between renin-angiotensin system (RAS) related gene polymorphisms, such as angiotensin converting enzyme (ACE) insertion/deletion (I/D), angiotensinogen (AGT) M253T and angiotensin II type 1 receptor (AT1R) A1166C, and the effect of quinapril, an ACE inhibitor with high tissue-binding affinity, on preventing restenosis after percutaneous coronary intervention (PCI). A total of 253 patients successfully treated for coronary artery disease were randomly assigned to quinapril or control. Of the 215 patients who completed the follow-up, we determined gene polymorphisms in 204 patients with 241 lesions who provided blood samples for genotype determination. In the control, the ACE D homozygotes showed a smaller minimal lumen diameter (MLD) at follow-up (P=0.063). The other two genotypes of AGT and AT1R did not affect restenosis after PCI. According to quinapril treatment, the AGT T homozygotes significantly showed a beneficial effect of quinapril on MLD (P=0.013) and late lumen loss (P=0.013). The ACE I homozygotes also exhibited beneficial effects of quinapril on larger MLD (P=0.065). The AT1R genotype did not influence the quinapril effect. In conclusion, the AGT T homozygotes might benefit from effects of quinapril on preventing restenosis after PCI.

Influence of type 2 diabetes mellitus on cardiovascular disease mortality: findings from the Hawaii-Los Angeles-Hiroshima study.

The present study addressed whether diabetes mellitus was a strong risk factor for cardiovascular disease (CVD) death. Between 1976 and 1984, 927 (404 men) Japanese-Americans in Hawaii aged 40-79 years participated at baseline examination including a 75 g oral glucose tolerance test. Diabetes was defined as fasting serum glucose >or=140 mg/dl, 2 h postload glucose >or=180 mg/dl, or the use of drugs for diabetes. Causes of death were classified by ICD-9 codes on the reports from the Hawaii State Public Health Bureau. Until 1994, 178 individuals suffered death; 81 were attributed to CVD and 43 to coronary heart disease (CHD). The age-adjusted and coronary risk factors-adjusted relative risks for CHD and CVD mortality were significant for diabetes both in men and women. The impact of diabetes on CHD mortality was greater for women. However, no gender difference in the contribution of diabetes to fatal CVD was observed. Serum fasting glucose levels tended to be associated with CHD death and were associated with CVD death in diabetic subjects. In conclusion, diabetes is a strong independent risk factor for CVD mortality in Japanese-American men and women. Hyperglycemia is associated with CVD mortality in diabetic subjects.

Plasma levels of oxidized low density lipoprotein are associated with stable angina pectoris and modalities of acute coronary syndrome.

The role of plasma levels of oxidized low density lipoprotein (OxLDL) in the development of coronary heart disease (CHD) has not been fully elucidated. We examined the relationship among plasma levels of OxLDL, measured by an enzyme immunoassay using an antibody against OxLDL (FOH1a/DLH3) and apolipoprotein B, CHD, and modalities at the onset of acute coronary syndrome (ACS). A total of 115 individuals who underwent coronary angiography were studied. Of these, 21 patients complicated with extracoronary cardiovascular diseases were excluded. Consequently, 94 patients (63 men) (ACS: 23, stable angina pectoris (SAP): 46, and normal coronary artery (NCA):25) were eligible for inclusion in the study. Elevated plasma levels of OxLDL were associated with CHD, especially with ACS. In patients with NCA, hypertension was associated with plasma OxLDL. Plasma levels of OxLDL were significantly higher in patients with new-onset type ACS than in those with worsening type ACS (2.98 versus 1.53 mg/dL, P = 0.002). In conclusion, plasma levels of OxLDL are associated with CHD and significantly higher in patients with new-onset ACS. The findings of the present study suggest that plasma OxLDL can be a marker of the development of CHD and modalities of ACS.