Daisuke Kanda

Angiotensin-Converting Enzyme Inhibitor Prevents the Worsening of Renal Function in the Late Phase after Percutaneous Coronary Intervention.

AIM The amount of contrast media and renal atheroemboli are risk factors for acute kidney injury after percutaneous coronary intervention (PCI). However, the chronic kidney injury after PCI has not been fully characterized. The purpose of this study was to investigate factors affecting renal function in the late phase after PCI by measuring serum Cystatin C (CysC). METHODS In 143 consecutive patients who underwent elective PCI, CysC was evaluated at baseline and at 9 months after PCI, and the percent change in CysC (%CysC) was calculated. The association between %CysC and baseline characteristics, including medication use, was assessed. RESULTS Of 143 patients, 86 had worsening renal function (WRF; %CysC ≥0), and 57 did not (non-WRF; %CysC <0). Only the use of angiotensin-converting enzyme inhibitor (ACEI) and baseline CysC were significantly different between WRF and non-WRF patients (15 vs. 40%, p=0.001 and 1.02±0.26 vs. 1.13±0.26 mg/L, p=0.015). In univariate analysis, the use of ACEI and CysC were negatively associated with WRF [Odds ratio (OR)=0.26, 95% confidence interval (CI)=0.12-0.57, p<0.001 and OR=0.20, 95% CI=0.05-0.73, p=0.015]. Furthermore, multivariate analysis revealed that the use of ACEI and CysC significantly correlated with WRF (OR=0.26, 95% CI=0.11-0.57, p<0.001 and OR=0.20, 95% CI=0.05-0.74, p=0.016). The %CysC in 36 patients with ACEI was significantly lower than that in 107 patients without ACEI [median: -3.8%; interquartile range (IQR), -11.0 to 4.2%; vs. median: 3.3%; IQR -2.9 to 11.0%, p=0.001]. CONCLUSION The use of ACEI was associated with lower CysC after PCI, suggesting that ACEI prevents worsening of renal function in late phase after PCI.

Prospective Study on the Incidence of Cerebrovascular Disease After Coronary Angiography

Aim: Previous studies have reported a 10.2%–22% rate of silent cerebral infarction and a 0.1% –1% rate of symptomatic cerebral infarction after coronary angiography (CAG). However, the risk factors of cerebral infarction after CAG have not been fully elucidated. For this reason, we investigated the incidence and risk factors of CVD complications within 48 h after CAG using magnetic resonance imaging (MRI) (Diffusion-weighted MRI) at Kagoshima University Hospital. Methods: From September 2013 to April 2015, we examined the incidence and risk factors, including procedural data and patients characteristics, of cerebrovascular disease after CAG in consecutive 61 patients who underwent CAG and MRI in our hospital. Results: Silent cerebral infarction after CAG was observed in 6 cases (9.8%), and they should not show any neurological symptoms of cerebral infarction. Only prior coronary artery bypass grafting (CABG) was more frequently found in the stroke group (n = 6) than that in the non-stroke group (n = 55); however, no significant difference was observed (P = 0.07). After adjusting for confounders, prior CABG was a significant independent risk factor for the incidence of stroke after CAG (odds ratio: 11.7, 95% confidence interval: 1.14–129.8, P = 0.04). Conclusions: We suggested that the incidence of cerebral infarction after CAG was not related to the catheterization procedure per se but may be caused by atherosclerosis with CABG.

Validity of a Novel Method for Estimating Low-Density Lipoprotein Cholesterol Levels in Cardiovascular Disease Patients Treated with Statins

Aim: The Friedewald equation is the standard method for estimating low-density lipoprotein cholesterol (LDL-C) levels [LDL-C(F)] and fixes the ratio of triglyceride (TG) to very LDL-C at 5. However, this has been reported to underestimate LDL-C, particularly in patients with LDL-C < 70 mg/dL. A novel method for LDL-C estimation [LDL-C(M)] using an adjustable factor instead of a fixed value of 5 has recently been proposed. The purpose of this study was to validate LDL-C(M) in Japanese patients with cardiovascular disease (CVD) treated with statins. Methods: In 385 consecutive CVD patients treated with statins, LDL-C(M) and LDL-C(F) levels were compared with directly measured LDL-C [LDL-C(D)]. Results: Mean LDL-C(D), LDL-C(F), and LDL-C(M) were 81.7 ± 25.5, 76.4 ± 24.6, and 79.9 ± 24.5 mg/dL, respectively. In all patients, both LDL-C(F) and LDL-C(M) were significantly correlated with LDL-C(D) [LDL-C(F) vs. LDL-C(D): R = 0.974, p < 0.001; LDL-C(M) vs. LDL-C(D): R = 0.987, p < 0.001]. In patients with LDL-C(D) < 70 mg/dL, LDL-C(M) showed a better correlation with LDL-C(D) compared with LDL-C(F) [LDL-C(M) vs. LDL-C(D): R = 0.935, p < 0.001; LDL-C(F) vs. LDL-C(D): R = 0.868, p < 0.001]. In contrast, the correlation of LDL-C(D) with LDL-C(M) or LDL-C(F) was similar in patients with LDL-C(D) ≥ 70 mg/dL. Conclusions: In Japanese patients with CVD treated with statins, LDL-C level estimated by this novel method might be more accurate than those estimated using the Friedewald equation for LDL-C levels < 70 mg/dL.

BRACHIAL-ANKLE PULSE WAVE VELOCITY CORRELATED WITH AN ENDOTHELIUM-INDEPENDENT VASODILATION IN CONDUIT CORONARY ARTERY

Methods: Seventy-one consecutive patients (49 men, 22 women, mean age 61±13 years) with normal or mildly diseased coronary arteries were enrolled. Vascular reactivity was assessed by intracoronary administration of papaverine, acetylcholine, and nitroglycerin using a Doppler guidewire. A bolus of papaverine induces an endothelium-independent vasodilator in resistance coronary arteries, infusion of acetylcholine induces an endothelium-dependent vasodilator in resistance and conduit coronary arteries, and a bolus of nitroglycerin induces an endothelium-independent vasodilator in conduit coronary arteries. BaPWV was measured using automated device.