ABSTRACT
Patients with peripheral artery disease (PAD) are at high risk of major adverse limb events (MALEs) and major adverse cardiovascular events (MACEs). CHA2DS2-VASc is a prognostic score for atrial fibrillation stroke risk; however, no study has evaluated its predictive ability for MALEs and MACEs in PAD patients who underwent percutaneous transluminal angioplasty. We conducted a retrospective cohort study on patients from Taiwan with PAD. The patients were stratified into four risk groups based on their modified CHA2DS2-VASc score. Cox proportional hazard models, 10-fold cross-validation, and receiver operating characteristic (ROC) analyses were utilized to evaluate the predictive ability of CHA2DS2-VASc for MALEs, MACEs, and MALEs + MACEs. Kaplan-Meier analysis estimated the survival probability of the risk groups. CHA2DS2-VASc was found to be a significant predictor of MACEs (hazard ratio (HR) 3.52 (95% confidence interval (95% CI) 1.00-12.12; p = 0.048), HR 4.18 (95% CI 1.19-14.36; p = 0.023), and HR 5.08 (95% CI 1.49-17.36; p = 0.009), for moderate-, high-, and very high-risk groups, respectively), while for MALEs and MALEs + MACEs, significance was achieved only for the high-risk group using a univariate model. For the multivariate adjusted model, the score was found to be a significant predictor of MACEs for only the very high-risk group, with an HR of 4.67 (95% CI 1.03-21.09; p = 0.045). The score demonstrated an AUC > 0.8, good discrimination (c-index > 0.8), and good calibration for predicting MACEs. However, it failed to achieve good performance for predicting MALEs and MALEs + MACEs. Based on all of the findings, CHA2DS2-VASc could potentially serve as a risk stratification score for predicting MACEs in patients with PAD, but it failed to qualify as a good predictor for MALEs.
ABSTRACT
AIMS: Hypertrophic cardiomyopathy (HCM) is an inheritable disease that leads to sudden cardiac death and heart failure (HF). Sarcomere mutations (SMs) have been associated with HF. However, the differences in ventricular function between SM-positive and SM-negative HCM patients are poorly characterized. METHODS AND RESULTS: Of the prospectively enrolled 374 unrelated HCM patients in Taiwan, 115 patients underwent both 91 cardiomyopathy-related gene screening and cardiovascular magnetic resonance (45.6 ± 10.6 years old, 76.5% were male). Forty pathogenic/likely pathogenic mutations were identified in 52 patients by next-generation sequencing. The SM-positive group were younger at first cardiovascular event (P = 0.04) and progression to diastolic HF (P = 0.02) with higher N-terminal pro-brain natriuretic peptide (NT-proBNP) [New York Heart Association (NYHA) Class III/IV symptoms with left ventricular ejection fraction > 55%] than the SM-negative group (P < 0.001). SM-positive patients had a greater extent of late gadolinium enhancement (P = 0.01), larger left atrial diameter (P = 0.03), higher normalized peak filling rate (PFR) and PFR ratio, and a greater reduction in global longitudinal strain than SM-negative patients (all P ≤ 0.01). During mean lifelong follow-up time (49.2 ± 15.6 years), SM-positive was a predictor of earlier HF (NYHA Class III/IV symptoms) after multivariate adjustment (hazard ratio 3.5; 95% confidence interval 1.3-9.7; P = 0.015). CONCLUSION: SM-positive HCM patients had a higher extent of myocardial fibrosis and more severe ventricular diastolic dysfunction than those without, which may contribute to earlier onset of advanced HF, suggesting the importance of close surveillance and early treatment throughout life.
ABSTRACT
A 25-year-old previously healthy male presented to our emergency room with acute chest pain and ventricular arrhythmia-related cardiac arrest. ST elevation myocardial infarction was diagnosed and coronary angiography revealed diffuse critical narrowing from the proximal to the distal left anterior descending artery. Diffuse intramural hematoma was demonstrated on intravascular ultrasound. Two stents were placed to cover the whole dissection length and flow was successfully restored. Spontaneous coronary artery dissection can be a fatal event and could be mistaken for atherosclerotic plaque or coronary spasm rather than luminal compression on coronary angiography and intravascular imaging is helpful in this condition.
