Hitone Tateyama

Impact of Cilostazol on Restenosis After Percutaneous Coronary Balloon Angioplasty

BACKGROUND Restenosis after percutaneous transluminal coronary (balloon) angioplasty (PTCA) remains a major drawback of the procedure. We previously reported that cilostazol, a platelet aggregation inhibitor, inhibited intimal proliferation after directional coronary atherectomy and reduced the restenosis rate in humans. The present study aimed to determine the effect of cilostazol on restenosis after PTCA. METHODS AND RESULTS Two hundred eleven patients with 273 lesions who underwent successful PTCA were randomly assigned to the cilostazol (200 mg/d) group or the aspirin (250 mg/d) control group. Administration of cilostazol was initiated immediately after PTCA and continued for 3 months of follow-up. Quantitative coronary angiography was performed before PTCA and after PTCA and at follow-up. Reference diameter, minimal lumen diameter, and percent diameter stenosis (DS) were measured by quantitative coronary angiography. Angiographic restenosis was defined as DS at follow-up >50%. Eligible follow-up angiography was performed in 94 patients with 123 lesions in the cilostazol group and in 99 patients with 129 lesions in the control group. The baseline characteristics and results of PTCA showed no significant difference between the 2 groups. However, minimal lumen diameter at follow-up was significantly larger (1.65+/-0.55 vs 1.37+/-0.58 mm; P<0.0001) and DS was significantly lower (34.1+/-17.8% vs 45.6+/-19. 3%; P<0.0001) in the cilostazol group. Restenosis and target lesion revascularization rates were also significantly lower in the cilostazol group (17.9% vs 39.5%; P<0.001 and 11.4% vs 28.7%; P<0. 001). CONCLUSIONS Cilostazol significantly reduces restenosis and target lesion revascularization rates after successful PTCA.

Coronary angioplasty of chronic total occlusions with bridging collateral vessels: immediate and follow-up outcome from a large single-center experience.

OBJECTIVES The purpose of the present study was to assess the effect of bridging collateral vessels on the success of coronary angioplasty of chronic total occlusions in the context of state of the art technology and operator skill. BACKGROUND Coronary angioplasty of chronic total occlusions has been associated with relatively low success rates. Because the presence of bridging collateral vessels in chronic total occlusion has been reported to be the major predictive factor in procedural failure, angioplasty is often not recommended in patients with such vessels. METHODS Three hundred ninety-seven consecutive patients undergoing coronary angioplasty for chronic total occlusion were classified into two groups. Patients in group I had chronic total occlusion with bridging collateral vessels (97 patients, 109 total occlusions), and patients in group II had chronic total occlusion without such vessels (300 patients, 324 total occlusions). RESULTS The mean +/- SD duration of occlusion was 46 +/- 66 months (range 2 to 170) in group I and 27 +/- 39 months (range 2 to 112) in group II (p < 0.05, high power value 0.83, group I vs. group II). Angioplasty for single-vessel disease was performed in a smaller proportion of patients in group I than in group II (22% vs. 36%, p < 0.05; power value 0.77). Procedural success was achieved in 82 chronic total occlusions in group I and 270 chronic total occlusions in group II (75% vs. 83%, p = 0.07; power value 0.53). The rates of restenosis and reocclusion were 54% and 16%, respectively, for group I and 56% and 13%, respectively, for group II (p = 0.76, 0.46; power value 0.51, 0.47). Complications were minor with no Q wave infarction or requirement for urgent bypass surgery in either group. Of 81 patients with unsuccessful coronary angioplasty, 1 patient from group I (1%) and 3 patients from group II (1%) required pericardiocentesis because of cardiac tamponade. Guide wire manipulation did not impair the flow of bridging collateral channels in group I. CONCLUSIONS Coronary angioplasty can open chronic total occlusions, with or without bridging collateral channels, for safe and effective recanalization without major complications.

Characterization of immunoreactive human C-type natriuretic peptide in brain and heart.

Amino acid sequence of human C-type natriuretic peptide (CNP) has recently been deduced to be identical to those of porcine and rat CNPs in the bioactive unit of C-terminal 22 residues (CNP-22) (1). Thus, tissue concentrations and molecular forms of immunoreactive (ir-) CNP in human brain and heart were determined or characterized using a radioimmunoassay established for porcine CNP. In human brain (hypothalamus and medullapons), ir-CNP was detected at a concentration of 1.04 pmol/g, being about 25 times or 70 times higher than ir-atrial (A-type) natriuretic peptide (ANP) or ir-brain (B-type) natriuretic peptide (BNP). CNP was present mainly as CNP-53, with CNP-22 as well as 13K CNP (presumed to be pro-CNP) as minor components. In heart, 1 approximately 5 pmol/g of ir-CNP was detected in both atrium and ventricle, but this ir-CNP was shown to be derived from crossreactivity of ANP. These results demonstrated that human CNP functions exclusively in the central nervous system in contrast to ANP and BNP which mainly function in the circulation system.

Concentrations and molecular forms of human brain natriuretic peptide in plasma

Using a highly sensitive radioimmunoassay (RIA) system for human brain natriuretic peptide (BNP), immunoreactive (ir-) human BNP was found to be present in plasma, in addition to heart and brain tissue. Plasma concentrations of ir-BNP were 0.17-0.74 fmol/ml (mean: 0.35 fmol/ml) in normal young men, being about 1/17 of the plasma concentration of human atrial natriuretic peptide (ANP). In patients with heart disease, plasma concentration of ir-BNP increased about 100-fold (5.00-177.37 fmol/ml), being nearly comparable to that of ir-ANP, even though ANP concentration also increased about 7-fold. Two molecular forms of ir-BNP in plasma were identified as BNP-32 and gamma-BNP (pro-BNP), which are also found in cardiac atrium. In normal human plasma, gamma-BNP is the predominant molecular form, while the main form in cardiac atrium is BNP-32. These results suggest that biosynthesis and secretion of BNP are augmented in heart disease and that human BNP has a unique processing and metabolic system distinct from that of ANP.

Characterization of immunoreactive brain natriuretic peptide in human cardiac atrium.

Based on cDNA sequence data for human brain natriuretic peptide (BNP) precursor (1), a radioimmunoassay (RIA) system highly specific to human BNP (hBNP) was developed and used to characterize immunoreactive (ir-) hBNP in cardiac atrium. Gel filtration of ir-hBNP in atrium indicated that ir-hBNP was mainly comprised of two molecular forms of 13-15K and 4K. In reverse phase high performance liquid chromatography (HPLC), the low molecular weight (MW) ir-hBNP emerged as a single peak at an elution time identical to that of synthetic hBNP-32. The high MW ir-hBNP was also eluted as a single peak. On the other hand, tissue concentrations of ir-hBNP in cardiac atria were found to be 9.98-593.22 pmol/g in 13 specimens, being about 1/150 the concentration of ir-human atrial natriuretic peptide (hANP). These results demonstrate that hBNP is present as a peptide in human heart, suggesting that hBNP is secreted from heart and functions together with hANP as a hormone.

Impact of cilostazol on intimal proliferation after directional coronary atherectomy

Cilostazol, a novel platelet aggregation inhibitor, inhibits intimal proliferation in animal models. We randomly assigned 41 patients with lesions suitable for directional coronary atherectomy to the cilostazol group (200 mg/day) or the aspirin (250 mg/day) group. Medication was started before directional coronary atherectomy and was continued to a 6-month follow-up. Serial quantitative coronary angiography and intravascular ultrasound study were performed. Baseline characteristics were not different between the two groups. However, the minimal lumen diameter at follow-up was larger (2.33 +/- 0.60 mm vs 1.81 +/- 0.68 mm, p = 0.016) and the percent diameter stenosis (24.5% +/- 16.6% vs 40.9% +/- 21.0%, p = 0.010) was smaller in the cilostazol group. The change in vessel area was not different, but the percent plaque area at follow-up was smaller in the cilostazol group (55.7% +/- 11.2% vs 64.5% +/- 14.5%, p = 0.044). The restenosis rate was significantly lower in the cilostazol group (0% vs 26%, p = 0.020). We conclude that cilostazol appears to have an inhibitory effect on intimal proliferation after directional coronary atherectomy and may reduce restenosis.

Final results of the STent versus directional coronary Atherectomy Randomized Trial (START)

OBJECTIVES This study was designed to compare primary stenting with optimal directional coronary atherectomy (DCA). BACKGROUND No previous prospective randomized trial comparing stenting and DCA has been performed. METHODS One hundred and twenty-two lesions suitable for both Palmaz-Schatz stenting and DCA were randomly assigned to stent (62 lesions) or DCA (60 lesions) arm. Single or multiple stents were implanted with high-pressure dilation in the stent arm. Aggressive debulking using intravascular ultrasound (IVUS) was performed in the DCA arm. Serial quantitative angiography and IVUS were performed preprocedure, postprocedure and at six months. The primary end point was restenosis, defined as > or =50% diameter stenosis at six months. Clinical event rates at one year were also assessed. RESULTS Baseline characteristics were similar. Procedural success was achieved in all lesions. Although the postprocedural lumen diameter was similar (2.79 vs. 2.90 mm, stent vs. DCA), the follow-up lumen diameter was significantly smaller (1.89 vs. 2.18 mm; p = 0.023) in the stent arm. The IVUS revealed that intimal proliferation was significantly larger in the stent arm than in the DCA arm (3.1 vs. 1.1 mm ; p < 0.0001), which accounted for the significantly smaller follow-up lumen area of the stent arm (5.3 vs. 7.0 mm2; p = 0.030). Restenosis was significantly lower (32.8% vs. 15.8%; p = 0.032), and target vessel failure at one year tended to be lower in the DCA arm (33.9% vs. 18.3%; p = 0.056). CONCLUSIONS These results suggest that aggressive DCA may provide superior angiographic and clinical outcomes to primary stenting.

Hemodynamic, renal, and hormonal responses to alpha‐human atrial natriuretic peptide in patients with congestive heart failure

Hemodynamic, renal, and hormonal effects of intravenous bolus injection of 50 µg synthetic α‐human atrial natriuretic peptide (α‐hANP) were studied in eight patients with congestive heart failure. α‐hANP caused significant reductions in mean blood pressure and systemic vascular resistance. These responses were sustained up to 90 minutes and not accompanied by reflex tachycardia. Cardiac index and stroke volume index increased significantly at 90 minutes and pulmonary capillary wedge pressure, pulmonary arterial pressure, and mean right atrial pressure remained unchanged. Urine volume, urinary sodium excretion, creatinine clearance, and fractional excretion of sodium increased significantly, but fractional excretion of potassium and phosphate did not change. Elevated plasma renin activity, plasma aldosterone, and norepinephrine were suppressed after the injection of α‐hANP. The bolus injection of this peptide has moderately hypotensive, vasorelaxant, and natriuretic effects in patients with congestive heart failure.

Percutaneous myocardial ablation in double‐chamber right ventricle

Double‐chamber right ventricle (DCRV) exhibits intracavitary outflow obstruction. We report the first case of percutaneous myocardial ablation of DCRV in a 73‐year‐old patient. An alcohol‐induced conus branch occlusion provided the reduction of pressure gradient from 81 to 48 mm Hg and clinical improvement. This strategy may be an alternative therapy to surgery in the adult patients with DCRV. Cathet. Cardiovasc. Intervent. 49:97–101, 2000.

Specific Cardiomyopathy Caused by Multisystemic Lipid Storage in Jordan’s Anomaly

A 28-year-old Japanese man was admitted in 1996 with persistently high levels of serum creatine kinase (CK), glutamic oxaloacetic transaminase (GOT), and glutamic pyruvic transaminase (GPT). Physical examination revealed no skin disorder, but showed neurosensory hearing loss and early fatigability. The CK level was 1298 U/L (normal <90 U/L), the GOT level 73 U/L (normal <30 U/L), and the GPT level 79 U/L (normal <30 U/L) on admission. The patient’s serum carnitine level was 1.57 mg/dL (normal 1.22 to 1.86 mg/dL). Typical findings of Jordan’s …