Immediate and Evolutionary Recovery of Left Ventricular Diastolic Function after Transcatheter Aortic Valve Replacement: Comparison with Surgery.

PURPOSE: We aimed to compare the effect of transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (sAVR) on recovery of left ventricular (LV) diastolic function and afterload through serial echocardiographic examinations in patients with symptomatic high-risk severe aortic stenosis during early follow-up. MATERIALS AND METHODS: We included 38 patients undergoing TAVR (mean age, 80±6 years; male:female=18:20) and 27 patients undergoing sAVR (mean age, 78±3 years; male:female=12:15). We compared changes in the LV diastolic function and afterload before, immediately after, and 3 months after the procedure using serial transthoracic echocardiography. RESULTS: Immediately after the procedure, 16 (42%) and 3 (11%) patients in the TAVR and sAVR groups, respectively, showed rapid improvement in diastolic filling patterns. E wave to e' ratio (E/e') and right ventricular systolic pressure (RVSP) decreased significantly in the TAVR group (E/e': TAVR, from 24.6±12.9 to 20±9.5, p=0.048 vs. sAVR, from 21.5±9.4 to 20.64±6.4, p=0.361; RVSP: TAVR, 38.4±17.2 vs. 34±12.4, p=0.032 vs. sAVR, 32.2±11.7 vs. 30±6.8, p=0.27). After 3 months, diastolic grade distribution, E/e', and RVSP were similar. Valvuloarterial impedance significantly decreased immediately after the procedure in both groups (TAVR, from 5.1±1.4 to 3.1±1.0 vs. sAVR, from 4.5±1.5 to 3.1±0.8 mm Hg · mL⁻¹ · m⁻², p=0.001), but after 3 months, decreases were greater in the sAVR group (from 3.1±0.8 to 2.2±1.5 mm Hg · mL⁻¹ · m⁻², p=0.093). CONCLUSION: LV diastolic function improved more rapidly and earlier in patients treatment with TAVR than in patients treated with sAVR. These results might explicate the remarkable clinical improvement in improvements in advanced diastolic dysfunction immediately after the TAVR procedure than sAVR.

Switching from prasugrel to clopidogrel based on Cytochrome P450 2C19 genotyping in East Asian patients stabilized after acute myocardial infarction.

To evaluate the pharmacodynamic efficacy of de-escalating P2Y12 inhibition from prasugrel to clopidogrel based on cytochrome P450 (CYP) 2C19 genotyping, we genotyped 50 Korean patients with AMI who underwent percutaneous coronary intervention (PCI) for CYP2C19 *2,*3, or *17 using real-time PCR. They were discharged on prasugrel 10 mg daily. A control group of 48 AMI patients who underwent PCI and were discharged on clopidogrel but did not undergo genotyping was identified retrospectively. Based on genotyping results available at 3 weeks, 12 patients found to have 2 copies of either CYP2C19 *2 or *3 loss of function alleles continued prasugrel while the remaining 38 patients switched to clopidogrel 75 mg daily. The rate of patients within the therapeutic window (TW) of on-treatment platelet reactivity (OPR), 85

Efficacy of cilostazol on uncontrolled coronary vasospastic angina: a pilot study.

BACKGROUND: Although an angina attack by vasospastic angina (VSA) can usually be relieved or controlled with nitrates and calcium channel blockers (CCBs), there are some patients who cannot be controlled even by higher doses and combinations of these drugs. Cilostazol is a selective inhibitor of phosphodiesterase 3 that increases intracellular cyclic adenosine monophosphate (cAMP) contents. A stimulation of cAMP signal transduction increases coronary nitric oxide production. We examined whether cilostazol improved angina symptoms in patients with VSA uncontrolled by conventional treatment. METHODS: This study was conducted in a prospective, multicenter, nonrandomized manner. The subject consisted of 21 patients (13 men, 57 ± 9 year-old) who were diagnosed with VSA and had at least two angina attacks during the past 1 week despite of conventional medications such as CCBs and/or nitrates. They took cilostazol 100 mg twice daily for 2 weeks in addition to the conventional medications. The patients recorded the frequency of angina attack and wrote down the numeric rating scale of a "severity of angina attack" while taking conventional medications and cilostazol for 2 weeks, and also recorded an averaged scale or total number of event during the last week at the time of the assessment. Using the Wilcoxon rank-sum test, we compared the changes in the scores of frequency and severity of angina attack before and after adding cilostazol to the conventional medications. RESULTS: After adding cilostazol to the conventional medications, there were 78.9% relative reduction of the score of angina intensity and 73.5% of angina frequency (P < 0.001). There were four patients (19%) who were forced to stop cilostazol due to headache as an adverse event. CONCLUSIONS: Cilostazol appears to be an effective therapy in VSA uncontrolled with conventional medical treatment. A further prospective, randomized, placebo-controlled study will be needed to validate this result.

Preventive strategies of renal insufficiency in patients with diabetes undergoing intervention or arteriography (the PREVENT Trial).

Few studies have compared the ability of sodium bicarbonate plus N-acetylcysteine (NAC) and sodium chloride plus NAC to prevent contrast-induced nephropathy (CIN) in diabetic patients with impaired renal function undergoing coronary or endovascular angiography or intervention. Diabetic patients (n = 382) with renal disease (serum creatinine ≥1.1 mg/dl and estimated glomerular filtration rate <60 ml/min/1.73 m(2)) were randomly assigned to receive prophylactic sodium chloride (saline group, n = 189) or sodium bicarbonate (bicarbonate group, n = 193) before elective coronary or endovascular angiography or intervention. All patients received oral NAC 1,200 mg 2 times/day for 2 days. The primary end point was CIN, defined as an increase in serum creatinine >25% or an absolute increase in serum creatinine ≥0.5 mg/dl within 48 hours after contrast exposure. There were no significant between-group differences in baseline characteristics. The primary end point was met in 10 patients (5.3%) in the saline group and 17 (9.0%) in the bicarbonate group (p = 0.17), with 2 (1.1%) and 4 (2.1%), respectively, requiring hemodialysis (p = 0.69). Rates of death, myocardial infarction, and stroke did not differ significantly at 1 month and 6 months after contrast exposure. In conclusion, hydration with sodium bicarbonate is not superior to hydration with sodium chloride in preventing CIN in patients with diabetic nephropathy undergoing coronary or endovascular angiography or intervention.

Recent insights into the mechanisms of vasospastic angina.

Coronary artery spasm plays an important role in the pathogenesis of many types of ischemic heart disease, not only in vasospastic angina but also in myocardial infarction and sudden death, particularly in the asian population. Patients with vasospastic angina are known to have defective endothelial function due to reduced nitric oxide bioavailability. Moreover, markers of oxidative stress and plasma levels of C-reactive protein are elevated. Smoking, polymorphysms of endothelial nitric oxide synthetase (eNOS), and low-grade inflammation have been regarded as the most important risk factors for vasospastic angina. The recent body of evidence indicates that RhoA and its down stream effector, ROCK/Rho-kinase, are associated with hypercontraction of vascular smooth muscle of the coronary artery and regulation of eNOS activity. Thus, endothelial dysfunction through abnormalities of eNOS and enhanced contractility of vascular smooth muscle in coronary artery segments are considered major mechanisms in vasospastic angina. However, the precise mechanisms for coronary vasospasm are not well understood. This article will review current understanding of the mechanism of coronary artery spasm.