Left ventricular twist in hypertrophic cardiomyopathy : Predictor of nonsustained ventricular tachycardia.

BACKGROUND: We investigated the efficacy of clinical and classic echocardiographic parameters in predicting the occurrence of nonsustained ventricular tachycardia (NsVT) in patients with hypertrophic cardiomyopathy (HCM). METHODS: The study comprised 59 patients with HCM (47 male, [80%]; mean age, 48.48 ± 14.16 years). Clinical, electrocardiographic, as well as classic two-dimensional and speckle-tracking echocardiography (STE) data were collected. All patients had Holter monitoring within 24-72 h of the echocardiographic examination. NsVT was defined as three or more consecutive premature wide QRS complexes with a heart rate of > 100 bpm. The patient population was categorized into groups based on the occurrence or absence of NsVT on the 24-h Holter recordings. RESULTS: NsVT was observed in 17 patients (29%). In these patients, higher twist (14.4 ± 3.8 vs.18 ± 7.9; p = 0.02), higher apical rotation (8.7 ± 4.2 vs. 12.2 ± 7; p = 0.02), higher sudden cardiac death risk score (4.4 ± 2.2 vs. 7 ± 3.3; p = 0.007), and decreased global longitudinal peak strain (GLPS; -12.8 ± 3.1 vs. -10.6 ± 2.8; p = 0.014) were observed. In the multivariate logistic regression analysis, including GLPS and twist, GLPS (Odds Ratio [OR]: 1.406; 95% CI: 1.087-1.818; p = 0.009) and twist (OR: 1.236; 95% CI: 1.056-1.446; p = 0.008) were found to be independent predictors of NsVT. In the receiver operating characteristic curve analysis, GLPS < -11.9% predicted NsVT with 82% sensitivity and 60% specificity (area under the curve [AUC]: 0.70; p = 0.014) and twist > 15.2° predicted NsVT with 70% sensitivity and 58% specificity (AUC: 0.69; p = 0.027). CONCLUSION: Decreased GLPS and increased twist were predictive of NsVT in HCM patients. Parameters that can easily be measured with STE can help detect patients who may develop arrhythmia.

HMGCR and ApoE mutations may cause different responses to lipid lowering statin therapy.

Coronary artery disease (CAD) and its complications are the major causes of death in the world. Although statins have been used to lower lipid levels in CAD patients, this goal can not be attained in 1/3 of the patients. The objective of this study was to investigate whether common variations in HMG-CoA Reductase(HMGCR) and Apolipoprotein E (ApoE) genes involved in lipid and statin metabolism modify the effect of statins on serum lipid and lipoprotein concentrations in CAD patients.A hundred  CAD patients were enrolled into the study. At the beginning of the study biochemical measurements were performed to determine the baseline levels performed. Patients were treated with 40 mg atorvastatin for 2 months and biochemical measurements were repeated. According to the post-treatment, LDL-c levels,  patients were divided into 2 groups as non-responders and responders, respectively. The information regarding the risk factors such as smoking, alcohol consumption etc. were also obtained. DNA was isolated from peripheral blood. The presence of rs17244841 ve rs17238540 mutations in HMGCR and ε2, ε3 and ε4 variants of ApoE were determined by using RT-PCR. Results were evaluated statistically. HMGCR mutatations were mostly found in responders and ε4 variant of ApoE was mostly found in non-responders. It was also found that presence of HMGCR mutations causes a significant reduction in total cholesterol and LDL-c levels. Also presence of ε2 variant of ApoE causes a statistically significant increase in trigliseride levels. Our findings should be investigated with other researchers to clarify the mechanism.