LV Mass Independently Predicts Mortality and Need for Future Revascularization in Patients Undergoing Diagnostic Coronary Angiography.

OBJECTIVES: The goal of this study was to assess associations between left ventricular (LV) mass, all-cause mortality, and need for revascularization in patients undergoing coronary angiography. BACKGROUND: LV hypertrophy is associated with adverse cardiovascular outcomes in healthy subjects. However, its influence in those with known or suspected coronary artery disease is poorly understood. METHODS: A total of 3,754 patients (mean age 59.3 ± 13.1 years) undergoing invasive coronary angiography and cardiac magnetic resonance (CMR) (mean interval 1.0 ± 1.5 months) were studied. LV mass and volumes were determined from cine images and indexed to body surface area. Analyses were adjusted for CMR variables, medical comorbidities, and severity of coronary artery disease (Duke Jeopardy Score) and were stratified to LV function. RESULTS: At a median of 44.9 months, 315 patients (8.4%) died and 168 patients (4.5%) underwent revascularization. Multivariable analysis showed that each 10 g/m2 increase in LV mass index was associated with a 6% greater risk of mortality (hazard ratio: 1.06; 95% confidence interval [CI]: 1.01 to 1.11; p = 0.02) and a 10% greater need for revascularization (hazard ratio: 1.10; 95% CI: 1.04 to 1.17; p < 0.01). According to pre-defined thresholds, moderate to severe hypertrophy was associated with a 1.7-fold risk of mortality (95% CI: 1.2 to 2.3) and 1.8-fold need for revascularization (95% CI: 1.18 to 2.67). These findings were predominantly observed in those with a left ventricular ejection fraction >35% with respective hazard ratios of 2.93 (95% CI: 1.92 to 4.47) and 2.20 (95% CI: 1.21 to 3.98). CONCLUSIONS: LV mass index is an independent predictor of all-cause mortality and need for revascularization. This finding establishes relevance for LV mass measurements in clinical decision-making surrounding both the need and timing of revascularization in this population.

Relation Between Family History of Premature Coronary Artery Disease and the Risk of Death in Patients With Coronary Artery Disease.

Family history (FHx) of premature coronary artery disease (CAD) is a risk factor for development of incident cardiovascular disease. However the association between FHx and outcomes in patients with established CAD is unclear. We followed 84,373 patients with angiographic CAD enrolled in the inclusive Alberta Provincial Project for Outcomes Assessment in Coronary Heart Disease registry between April 2002 and March 2013. Overall, 25,566 (30%) self-reported an FHx of CAD, defined as a first-degree relative with premature CAD (men, age <55 years; women, age <65 years). We tested the association between FHx and all-cause mortality using multivariable Cox proportional hazards regression. After adjusting for baseline differences in clinical characteristics, indication, and extent of CAD, FHx was associated with reduced all-cause mortality over a median 5.6 years in follow-up (hazard ratio [HR] 0.77 [95% CI 0.73 to 0.80]). The magnitude of this protective association was weaker in those with versus without a previous myocardial infarction (HR 0.87 [95% CI 0.81 to 0.93] versus 0.72 [0.69 to 0.76], interaction p <0.0001) and slightly stronger in those presenting with versus without an acute coronary syndrome (HR 0.74 [0.70 to 0.79] versus 0.80 [0.75 to 0.85], interaction p = 0.08). There was attenuation of association with increasing age, but FHx remained protective even in those aged older than 80 years (HR 0.86 [0.77 to 0.95]). In conclusion, in patients with angiographic CAD, self-reported FHx of premature CAD is associated with improved long-term survival rate, independent of clinical characteristics, mode of presentation, and extent of disease. Further investigation of potential patient- and system-level mediators of this seemingly paradoxical relation is required.

25-Hydroxyvitamin D status, arterial stiffness and the renin-angiotensin system in healthy humans.

Vitamin D deficiency is associated with increased arterial stiffness. We sought to clarify the influence of vitamin D in modulating angiotensin II-dependent arterial stiffness. Thirty-six healthy subjects (33 ± 2 years, 67% female, mean 25-hydroxyvitamin D 69 ± 4 nmol/L) were studied in high salt balance. Arterial stiffness, expressed as brachial pulse wave velocity (bPWV) and aortic augmentation index (AIx), was measured by tonometry at baseline and in response to angiotensin II infusion (3 ng/kg/min × 30 min then 6 ng/kg/min × 30 min). The primary outcome was change in bPWV after an angiotensin II challenge. Results were analyzed according to plasma 25-hydroxyvitamin D status: deficient (<50 nmol/L) and sufficient (≥ 50 nmol/L). There were no differences in baseline arterial stiffness between vitamin D deficient (25-hydroxyvitamin D 40 ± 2 nmol/L) and sufficient (25-hydroxyvitamin D 80 ± 4 nmol/L) groups. Compared with sufficient vitamin D status, vitamin D deficiency was associated with a decreased arterial response to angiotensin II challenge (Δbrachial pulse wave velocity: 0.48 ± 0.44 m/s versus 1.95 ± 0.22 m/s, p=0.004; Δaortic augmentation index: 9.4 ± 3.4% versus 14.2 ± 2.7%, p=0.3), which persisted for brachial pulse wave velocity response after adjustment for covariates (p=0.03). Vitamin D deficiency is associated with increased arterial stiffness in healthy humans, possibly through an angiotensin II-dependent mechanism.