ObjectiveThe accuracy of various 10-year cardiovascular disease (CVD) risk calculators in Indians may not be the same as in other populations. Present study was conducted to compare the various calculators for CVD risk assessment and statin eligibility according to different guidelines.MethodsConsecutive 1110 patients who presented after their first myocardial infarction were included. Their CVD risk was calculated using Framingham Risk score- Coronary heart disease (FRS-CHD), Framingham Risk Score- Cardiovascular Disease (FRS-CVD), QRISK2, Joint British Society risk calculator 3 (JBS3), American College of Cardiology/American Heart Association (ACC/AHA), atherosclerotic cardiovascular disease (ASCVD) and WHO risk charts, assuming that they had presented one day before cardiac event for risk assessment. Eligibility for statin uses was also looked into using ACC/AHA, NICE and Canadian guidelines.ResultsFRS-CVD risk assessment model has performed the best as it could identify the highest number of patients (51.9%) to be at high CVD risk while WHO and ASCVD calculators have performed the worst (only 16.2% and 28.3% patients respectively were stratified into high CVD risk) considering 20% as cut off for high risk definition. QRISK2, JBS3 and FRS-CHD have performed intermediately. Using NICE, ACC/AHA and Canadian guidelines; 76%, 69% and 44.6% patients respectively were found to be eligible for statin use.ConclusionFRS-CVD appears to be the most useful for CVD risk assessment in Indians, but the difference may be because FRS-CVD estimates risk for several additional outcomes as compared with other risk scores. For statin eligibility, however, NICE guideline use is the most appropriate.
Addition of Ivabradine to standard therapy in patients with DCM and symptomatic HF and targeting a heart rate<70/min improves symptoms, quality of life and various echocardiographic parameters.
Patients with CKD have endothelial dysfunction as evidenced by reduced FMD. Decreased FMD indicating worsening endothelial function was noted with increasing severity of CKD. Within three months of RT, there was significant improvement in FMD, while NMD values did not change.
RationaleMutations in MYBPC3 encoding cardiac myosin binding protein C are common genetic cause of hereditary cardiac myopathies. An intronic 25-bp deletion in MYBPC3 at 3′ region is associated with dilated (DCM) and hypertrophic (HCM) cardiomyopathies in Southeast Asia. However, the frequency of MYBPC3 25 bp deletion and associated clinical presentation has not been established in an unrelated cohort of left ventricular dysfunction (LVD) secondary to coronary artery disease (CAD) patients.ObjectiveWe sought to determine the role of MYBPC3 25 bp polymorphism on LVD in two cohorts of CAD patients.Methods and ResultsThe study included 265 consecutive patients with angiographically confirmed CAD and 220 controls. MYBPC3 25 bp polymorphism was determined by polymerase chain reaction. Our results showed that carrier status of MYBPC3 25 bp deletion was associated with significant compromised left ventricle ejection fraction (LVEF ≤45) in CAD patients (p value = <0.001; OR = 4.49). To validate our results, we performed a replication study in additional 140 cases with similar clinical characteristics and results again confirmed consistent findings (p = 0.029; OR = 3.3). Also, presence of the gene deletion did not have significant association in CAD patients with preserved ejection fraction (LVEF>45) (p value = 0.1; OR = 2.3).ConclusionThe frequency of MYBPC3 DW genotype and D allele was associated with compromised LVEF implying that genetic variants of MYBPC3 encoding mutant structural sarcomere protein could increase susceptibility to left ventricular dysfunction. Therefore, 25 bp deletion in MYBPC3 may represent a genetic marker for cardiac failure in CAD patients from Southeast Asia.
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