J.-L. Lin

Renin-angiotensin system gene polymorphisms and diastolic heart failure

Background  Diastolic heart failure (DHF) refers to an abnormality of diastolic distensibility, filling or relaxation of the left ventricle. The genetic study of DHF is scarce in the literature. The association of renin‐angiotensin system (RAS) and DHF are well known. We hypothesized that RAS genes might be the susceptible genes for DHF and conducted a case‐control study to prove the hypothesis.

Statin use reduces the risk of dementia in elderly patients: a nationwide data survey and propensity analysis

The objective of this study was to examine the association between the use of statins and the risk of newly diagnosed dementia in an elderly population.

Association between Genetic Polymorphisms in the Renin-Angiotensin System and Systolic Heart Failure Revised by a Propensity Score-Based Analysis

Objectives: The objective of this study is to identify possible genetic polymorphisms of the renin-angiotensin system (RAS) in systolic heart failure (sHF). Methods: A total of 509 patients were enrolled into this study. A non-parsimonious multivariable logistic regression model that incorporated potential risk factors was applied to calculate the propensity score for developing sHF. A 1:1 case-control selection process was made according to the rank of propensity. The six genetic polymorphisms of angiotensinogen (AGT), including T174M, M235T, G-6A, A-20C, G-152A, and G-217A, and angiotensin-converting enzyme (ACE) gene I/D polymorphism were typed by polymerase chain reaction and DNA sequencing technique. Results: The CC genotype at T174M was positively associated with sHF (OR 2.81, 95% CI 1.20–6.61, p = 0.018). The GG genotype at G-152A was also positively associated with the presence of sHF (OR 6.25, 95% CI 1.54–25.4, p = 0.010). OR of the ACE DD genotype for sHF, as compared with ACE II genotype, was 1.37 (p = 0.475), and OR for ID genotype compared with II genotype was 5.95 for sHF (95% CI 2.16–16.4, p = 0.001). Conclusions: The exploration of these RAS genes related to sHF may provide a more targeted and tailored treatment of sHF.

A functional variant in the promoter region regulates the C‐reactive protein gene and is a potential candidate for increased risk of atrial fibrillation

Abstract.  Chang S‐N, Tsai C‐T, Wu C‐K, Lee J‐K, Lai L‐P, Huang S‐W, Huang L‐Y, Tseng C‐D, Lin J‐L, Chiang F‐T, Hwang J‐J (National Taiwan University Hospital Yun‐Lin Branch, Yun‐Lin; National Taiwan University Hospital, Taipei; National Taiwan University Hospital, Taipei; Institute of Pharmacology, Taipei; and Graduate Institute of Biomedical Engineering, Taipei, Taiwan). A functional variant in the promoter region regulates the C‐reactive protein gene and is a potential candidate for increased risk of atrial fibrillation. J Intern Med 2012; 272: 305–315.

New electrocardiographic criteria for the differentiation between counterclockwise and clockwise atrial flutter: correlation with electrophysiological study and radiofrequency catheter ablation

Objective To develop new electrocardiographic (ECG) criteria for the differentiation between counterclockwise and clockwise atrial flutters. Background Traditionally, the ECG differentiation between counterclockwise and clockwise atrial flutters is based on the flutter wave polarity in the inferior leads. However, determination of flutter wave polarity is subjective and sometimes difficult, especially in flutter waves of undulating pattern. Patients The study comprised 37 consecutive patients with drug resistant atrial flutter; 30 had counterclockwise and 17 had clockwise atrial flutter (10 had both forms of atrial flutter). The isthmus dependence was confirmed by entrainment study and catheter ablation. The ECG patterns of both types of atrial flutter were compared and the flutter wave polarity in the inferior leads was determined by four independent cardiologists. Results The flutter wave polarity in the inferior leads appeared negative in 24, positive in one, and equivocal in five of the counterclockwise atrial flutters; polarity appeared negative in one, positive in 10, and equivocal in six of the clockwise atrial flutters. However, the aVF/lead I flutter wave amplitude ratio was > 2.5 in all counterclockwise but < 2.5 in all clockwise atrial flutters. The flutter wave nadirs in the inferior leads corresponded to the upstrokes in V1 in all counterclockwise atrial flutters, but corresponded to the downstrokes in V1 in all clockwise atrial flutters. Conclusions The flutter wave polarity in the inferior leads does not correlate well with the flutter wave rotating direction. However, counterclockwise and clockwise atrial flutters can be differentiated by new ECG criteria with high accuracy.