Background and Objectives：This study was designed to examine whether mesenchymal stem cells (MSCs) transduced with Akt are more resistant to apoptosis, and enhance cardiac repair, following the transplantation into infarcted porcine myocardium. Materials and Methods：The MSCs were separated and genetically engineered using ex-vivo myr-Akt-adenoviral gene transfer. The MSCs were delivered by intracoronary injection into infarcted porcine myocardium [group I (control: n=8), media only; group II (n=8), MSCs only; group III (n=8), MSCs modified with Akt]. Myocardial SPECT was performed before and 4 weeks after the MSC transplantation, with the pigs sacrificed for immunocytochemical staining and histological analyses for apoptosis and fibrosis. Results：The left ventricular ejection fractions (LVEF) were 44.7±16.6, 35.9±10.0 and 41.1±7.9% at first (each n=8), which changed to 29.7±8.5, 39.0±9.5 and 60.4±16.6% at 4 weeks after the MSC implantation in groups I, II and III, respectively. The myocardial infarction (MI) area changed from 17.6±9.2, 35.0±11.8 and 24.3±11.2% to 19.6±10.1, 27.2±13.9 and 7.4±5.3% in groups I, II and III, respectively. Transplantation of 1×10 7 cells into group II increased the ΔLVEF (-15.0±15.3 vs. 3.0±4.3%, n=8 in each, p=0.016) and decreased the ΔMI area (2.1±0.9 vs. 5.6±3.1%, n=8 in each, p=0.04) compared to those of the control group, and these changes were more significant in the ΔLVEF (19.3±15.7%, p=0.006) and ΔMI area (-16.4±6.1%, p=0.037) of group III. Conclusion：MSCs transduced with Akt enhance the repair of the injured area, prevent remodeling and restore systolic performance in infarcted porcine myocardium. (Korean Circulation J 2005;35:734-741) KEY WORDS：Myocardial infarction；Stem cells；Ventricular remodeling.서 론 최근 관상동맥질환은 선진국뿐만 아니라 한국에서도 급증 하여 성인 사망률의 주요한 원인이 되고 있다. 이러한 관상 동맥질환의 치료는 경피적 관상동맥 풍선 확장술과 스텐트 등으로 치료가 가능해 졌지만, 급성 심근경색증의 후유증으 논문접수일：2005년 5월 18일 수정논문접수일：2005년 9월 2일 심사완료일：2005년 9월 12일 교신저자：정명호, 501-757 광주광역시 동구 학동 8번지 전남대학교병원 심장센터, 전남대학교 의과학연구소 전화：(062) 220-6243·전송：(062) 228-7174·E-mail：myungho@chollian.net

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Two decades ago, it was recognized that lipoprotein(a) (Lp(a)) concentrations were elevated in patients with cardiovascular disease (CVD). However, the importance of Lp(a) was not strongly established due to a lack of both Lp(a)-lowering therapy and evidence that reducing Lp(a) levels improves CVD risk. Recent advances in clinical and genetic research have revealed the crucial role of Lp(a) in the pathogenesis of CVD. Mendelian randomization studies have shown that Lp(a) concentrations are causal for different CVDs, including coronary artery disease, calcified aortic valve disease, stroke, and heart failure, despite optimal low-density lipoprotein cholesterol (LDL-C) management. Lp(a) consists of apolipoprotein (apo) B100 covalently bound to apoA. Thus, Lp(a) has atherothrombotic traits of both apoB (from LDL) and apoA (thrombo-inflammatory aspects). Although conventional pharmacological therapies, such as statin, niacin, and cholesteryl ester transfer protein, have failed to significantly reduce Lp(a) levels, emerging new therapeutic strategies using proprotein convertase subtilisin-kexin type 9 inhibitors or antisesnse oligonucleotide technology have shown promising results in effectively lowering Lp(a). In this review we discuss the revisited important role of L(a) and strategies to overcome residual risk in the statin era.

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The potential cancer risk associated with long‐term exposure to angiotensin receptor blockers (ARBs) is still unclear. We assessed the risk of incident cancer among hypertensive patients who were treated with ARBs compared with patients exposed to angiotensin‐converting enzyme inhibitors (ACEIs), which are known to have a neutral effect on cancer development. Using the Korean National Health Insurance Service database, we analyzed the data of patients diagnosed with essential hypertension from January 2005 to December 2012 who were aged ≥40 years, initially free of cancer, and were prescribed either ACEI or ARB (n = 293,962). Cox proportional hazard model adjusted for covariates was used to evaluate the risk of incident cancer. During a mean follow‐up of 10 years, 24,610 incident cancers were observed. ARB use was associated with a decreased risk of overall cancer compared with ACEI use (hazard ratio [HR] 0.76, 95% confidence interval [CI] 0.72‐0.80). Similar results were obtained for lung (HR 0.73, 95% CI 0.64‐0.82), hepatic (HR 0.56, 95% CI 0.48‐0.65), and gastric cancers (HR 0.74, 95% CI 0.66‐0.83). Regardless of the subgroup, greater reduction of cancer risk was seen among patients treated with ARB than that among patients treated with ACEIs. Particularly, the decreased risk of cancer among ARB users was more prominent among males and heavy drinkers (interaction P < .005). Dose‐response analyses demonstrated a gradual decrease in risk with prolonged ARB therapy than that with ACEI use. In conclusion, ARB use was associated with a decreased risk of overall cancer and several site‐specific cancers.