Tatsuji Kanoh

Effectiveness of an antioxidant in preventing Restenosis after percutaneous transluminal coronary angioplasty : The Probucol Angioplasty Restenosis Trial

OBJECTIVES The Probucol Angioplasty Restenosis Trial was a prospective, randomized, controlled study that investigated the effectiveness of probucol therapy in reducing the rate of restenosis after percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND Antioxidants have an inhibitory effect on smooth muscle cell growth in experiments in vitro and in vivo, which suggests a possible pharmacologic effect on restenosis after PTCA. METHODS One hundred one patients were randomly assigned to receive 1,000 mg/day of probucol or control (no lipid-lowering) therapy 4 weeks before PTCA. After 4 weeks of premedication, both groups underwent PTCA. Probucol was continued until follow-up angiography 24 weeks after PTCA. Angiographic results were analyzed at a core laboratory by quantitative coronary angiography. RESULTS Dilation was successful in 46 of 50 patients in the probucol group and 45 of 51 in the control group. At follow-up angiography 24 weeks after angioplasty, angiographic restenosis occurred in 9 (23%) of 40 patients in the probucol group and 22 (58%) of 38 in the control group (p = 0.001). Minimal lumen diameter was 1.49 +/- 0.75 mm (mean +/- SD) in the probucol group and 1.13 +/- 0.65 mm in the control group (p = 0.02). Percent diameter stenosis at follow-up angiography in the probucol group was significantly lower than that in the control group (43.9% vs. 56.4%, p = 0.009). The late loss was 0.37 +/- 0.69 mm in the probucol group and 0.60 +/- 0.62 mm in the control group (p = 0.13). The loss/gain ratio was 0.32 +/- 0.74 in the probucol group and 0.56 +/- 0.81 in the control group (p = 0.059). Net gain was greater in the probucol group than in the control group (0.77 +/- 0.70 vs. 0.48 +/- 0.59 mm, p = 0.053). CONCLUSIONS Probucol administered beginning 4 weeks before PTCA appears to reduce restenosis rates.

Prevention of restenosis after percutaneous transluminal coronary angioplasty by reducing lipoprotein (a) levels with low-density lipoprotein apheresis

This study was designed to test the hypothesis that high plasma lipoprotein (a) (Lp[a]) levels are associated with an increase incidence of restenosis after angioplasty. Elective transluminal coronary angioplasty was performed in 66 patients (58 men and 8 women) aged 57 +/- 9 years (mean +/- SD). Two days before and 5 days after angioplasty, all patients underwent low-density lipoprotein (LDL) apheresis with a dextran sulfate cellulose column as an Lp(a) absorbent; 39 patients also received 10 mg of pravastatin and 1,500 mg of niacin daily. Restenosis was defined as a recurrent luminal stenosis of > or = 50% in a previously dilated segment. Median Lp(a) levels were reduced from 23.3 mg/dl before apheresis to 10.9 mg/dl after apheresis (p < 0.0001). Angiography performed 2 to 9 months after angioplasty revealed restenosis in at least 1 site in 38% of the 137 control patients and in 32% of the 66 patients who underwent apheresis. Restenosis also occurred in 37% of the patients who underwent apheresis alone and in 28% of the patients who also received pravastatin and niacin in combination with LDL apheresis. The restenosis rate was 21% in the 42 patients whose Lp(a) levels were significantly reduced > or = 50%, and in 50% of the 24 patients whose Lp(a) levels were significantly reduced < 50% (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of probucol on repeat revascularization rate after percutaneous transluminal coronary angioplasty (from the Probucol Angioplasty Restenosis Trial [PART])

To address the issue of whether probucol reduces clinical events after percutaneous transluminal coronary angioplasty (PTCA), we surveyed clinical status at 1 year after PTCA of 101 patients who had entered the Probucol Restenosis Angioplasty Trial. Repeat angioplasty at index lesions were required in 5 patients in the probucol group and in 12 in the control group, suggesting that probucol administered beginning 4 weeks before PTCA reduces repeat revascularization rates for 1 year.

Plasma Levels of Brain Natriuretic Peptide Increase in Patients with Idiopathic Bilateral Atrial Dilatation

Idiopathic bilateral atrial dilatation (IBAD) is an extremely rare anomaly and is usually associated with atrial fibrillation. Plasma levels of atrial natriuretic peptide (ANP) have been shown to increase in patients with atrial fibrillation. However, secretion of ANP and brain natriuretic peptide (BNP) in patients with IBAD remains unclear. We investigated the clinical features of 9 patients with IBAD and 16 age- and sex-matched patients with lone atrial fibrillation (LAF). Plasma levels of ANP and BNP were measured, and echocardiographic parameters were followed. Left (LAV) and right atrial volumes (RAV) were significantly higher in patients with IBAD than in patients with LAF (both p < 0.01). There were no differences between patients with IBAD and LAF in other echocardiographic parameters. The percent increases in LAV and RAV in patients with IBAD exceeded those in patients with LAF (both p < 0.01). Plasma levels of BNP and the BNP/ANP ratios in patients with IBAD were significantly higher than those in patients with LAF (both p < 0.01), but there was no significant difference in plasma levels of ANP. Regarding the clinical course of the patients with IBAD compared with those with LAF, the atrial volume increased gradually, and plasma levels of BNP were significantly higher. These findings suggested that IBAD was not only influenced by long-term atrial fibrillation, but also by subclinical left ventricular dysfunction.

Effectiveness of LDL-apheresis in preventing restenosis after percutaneous transluminal coronary angioplasty (PTCA): LDL-apheresis angioplasty restenosis trial (L-ART)

To investigate the efficacy of reducing plasma lipoprotein(a) (Lp(a)) as well as low density lipoprotein cholesterol (LDL-C) levels on the prevention of restenosis after PTCA, LDL-apheresis was attempted on a total of 54 patients at six institutions. LDL-apheresis using a dextran sulfate cellulose column has been proven to be an effective method for reducing both plasma Lp(a) and LDL-C levels. As a subgroup (apheresis-drug combined group), 29 of the 54 patients were given Pravastatin (HMG CoA reductase inhibitor) and Niceritrol (Nicotinic Acid) in addition to LDL-apheresis to maintain low plasma levels of both Lp(a) and LDL-C through the follow-up period of 5 months after PTCA. Patients whose plasma Lp(a) levels were reduced by more than 50% showed a lower restenosis rate than those whose plasma Lp(a) levels were reduced by less than 50% (21.2% vs. 52.4%, P = 0.0179), especially in patients with high plasma Lp(a) levels above 30 mg/dl where a much lower restenosis rate (15.0%) was observed. Furthermore, in the apheresis-drug combined group, the restenosis rate was 11.8% regardless of baseline plasma Lp(a) levels, including even those below 30 mg/dl. In conclusion, in patients with high plasma Lp(a) levels, a greater than 50% reduction in Lp(a) levels by LDL-apheresis is effective in preventing restenosis after PTCA. If the plasma Lp(a) reduction rate is greater than 50%, LDL-apheresis combined with lipid-lowering drugs such as niceritrol and pravastatin seems to be more effective, even in patients with low plasma Lp(a) levels.

Severe hypertriglyceridemia with plasma inhibitory factor(s) on lipoprotein lipase activity in a patient with a common Ser447–Ter LPL mutation

Severe hypertriglyceridemia is a major risk for acute pancreatitis. So far, several mutations on the lipoprotein lipase (LPL) gene causing type I hyperlipidemia have been identified. However, the common mutation Ser(447)-Ter has been recently proposed to have a lowering effect on serum triglyceride concentrations in the general population. In this study, we analyzed blood from a patient suffering from severe hypertriglyceridemia and pancreatitis with the mutation on the lipoprotein lipase gene, Ser(447)-Ter. The patients plasma showed inhibitory effects on the LPL activities from normal subjects. The bottom fraction separated by ultracentrifugation revealed enhanced effects as an inhibitory factor. The inhibitory effect observed in the bottom fraction was dose-dependent, stable at treatment of 65 degrees C for 30 min, and decreased significantly after being dialyzed using membranes with a cut-off molecular weight of 3500 or 6000 Da. The inhibitory effect was significantly higher when the post-heparin plasma was used from the patient or a subject with the same LPL mutation as an LPL source, compared to that from normal subjects. These results suggest that the patient has inhibitory factors in his plasma. Such inhibitory factors might cause severe hypertriglyceridemia in a case with the common mutation, which has been proposed to show the lowing effect on serum triglyceride concentrations in the general population.

A Case of Patent Ductus Arteriosus in an 88-Year-Old Patient

The patient was an 88-year-old woman. Chest X-rays revealed cardiomegaly, pulmonary congestion and pleural effusion. Electrocardiogram was sinus rhythm with STT changes. Transesophageal echocardiography showed the left ventricular ejection fraction 27% with pulmonary hypertension (67 mmHg). A shunt flow was noted from the descending aorta to the pulmonary artery with a Qp/Qs of 1.3. By day 7, the pleural effusion had dissipated. However, she later passed away. A literature search revealed that she is the oldest patient to be diagnosed with patent ductus arteriosus (PDA) by transesophageal echocardiography and that she is the third oldest reported case of PDA.

Aortic and mitral valvular calcification in patients undergoing hemodialysis for 10 years or more and their prognosis

Valvular disease in hemodialysis (HD) patients occurs at a younger age and progresses faster compared with valvular changes due to aging in the general population [1]. The following can be involved in the mechanism of valvular calcification: parathyroid abnormality, aging, long-term HD, and calcium deposits in valves due to calciumbased drug or phosphate binder [2]. Valvular calcification can develop due to hypertension, diabetes mellitus (DM), dyslipidemia, renal anemia, blood access, and infective endocarditis [3]. In this study, we examined aortic valvular calcification (AVC) and mitral valvular calcification (MVC) in patients undergoing HD for 10 years or more. Computed tomography (CT) and echocardiography were used to detect calcification. Comparison was made between valvular calcification and risk factors for arteriosclerosis. In addition, prognosis of valvular disease was examined. The subjectswere 41patients undergoingoutpatientHD for 10 years ormore. Theywere 29men and 12women (mean age: 60±8 years and meandurationofHD: 20±7 years). Theunderlyingdiseasewas chronic glomerulonephritis (CGN) in 28 patients (mean duration of hemodialysis: 23±7 years), DM in 10 patients (12±1 years), and polycystic kidney disease in 3 patients (22±1 years). Non-contrast enhanced cardiac CT was performed with a 0.5-second scan time and 1 cm scan width to examine the presence or absence of AVC and MVC. Visual assessmentwasperformed to evaluate the density of calcification. In the same period, the followingwasmeasured just before HD in the two-day break between HD sessions: total cholesterol, high density lipoprotein cholesterol (HDLC), triglyceride, postprandial glucose, hemoglobin A1c, calcium (Ca), phosphorus (P), Ca-P product, and parathyroid hormone. Echocardiography was also performed. All numerical data were expressed as means±standard deviation. Comparison of measurements between groups was performed using Students unpaired t test. A p-value of less than 0.05 was defined to be statistically significant. Table 1 shows patient characteristics by underlying disease. AVCwas difficult to differentiate from aortic calcification and MVC from left circumflex artery calcification. In both AVC and MVC, the motion of the heart caused plus and minus density artifacts. Thus, the apparent density of calcification differed from the actual density, and determination of severity of valvular calcificationwas difficult using CT. Therefore, accurate comparison could not be performed between the results of blood tests and the degree of calcification. CTexamination revealed AVC in 38 of 41 patients, andMVCwas seen in all patients.When the density was examined in each patient, the visually assessed density tended to International Journal of Cardiology 164 (2013) 123–128

Massive Pericardial Effusion in a Case of Acute Pericarditis with Slight ST-Segment Elevation of Short Duration.

We present the case of a 77-year-old woman who suffered from chest pain. Her white blood cell count was 10,200/μL and C-reactive protein level was 5.5 mg/dL. There was no electrocardiogram abnormality up to 5 hours after admission. At 15 hours, slight ST-segment elevation occurred, but this disappeared on day 4. Imaging revealed slight pericardial effusion. Nonsteroidal anti-inflammatory drugs and antibiotics were administered. However, the pericardial effusion, inflammatory response, and bilateral heart failure worsened. Pericardiotomy on day 6 released 350 mL of fluid, and symptoms improved. Viral pericarditis was assumed. Massive pericardial effusion is rare in cases of acute viral pericarditis, as is slight, short-duration ST-segment elevation.

Acute Myocardial Infarction with Severe ST Segment Elevation Treated with Percutaneous Coronary Intervention More than Two Days after Onset: A Case with Remarkable Recovery

The patient was a 65-year-old man with marked ST-elevation myocardial infarction. Cardiac catheterization revealed an occluded middle portion of the left anterior descending artery and no collateral circulation. Percutaneous coronary intervention (PCI) was performed, and ST elevation improved 5 days after PCI. Almost all electrocardiogram (ECG) findings were normal 6 months later. Echocardiographic findings were also normal. This case was very successful and unusual in that no ventricular aneurysm formed despite ST elevation continuing for a few days and that ECG and left ventricular function were nearly normal after PCI performed days after the onset in a case without collateral circulation.