Background: Coronary artery calcium (CAC) is an indicator of atherosclerosis, and the CAC score is a useful noninvasive assessment of coronary artery disease. Objective: To compare the risk of cardiovascular outcomes in patients with CAC > 0 versus CAC = 0 in asymptomatic and symptomatic population in patients without an established diagnosis of coronary artery disease. Methods: A systematic search of electronic databases was conducted until January 2018 for any cohort study reporting cardiovascular events in patients with CAC > 0 compared with absence of CAC. Results: Forty-five studies were included with 192 080 asymptomatic 32 477 symptomatic patients. At mean follow-up of 11 years, CAC > 0 was associated with an increased risk of major adverse cardiovascular and cerebrovascular events (MACE) compared to a CAC = 0 in asymptomatic arm [pooled risk ratio (RR) 4.05, 95% confidence interval (CI) 2.91–5.63, P < 0.00001, I ² = 80%] and symptomatic arm (pooled RR 6.06, 95% CI 4.23–8.68, P < 0.00001, I ² = 69%). CAC > 0 was also associated with increased risk of all-cause mortality in symptomatic population (pooled RR 7.94, 95% CI 2.61-24.17, P < 0.00001, I ² = 85%) and in asymptomatic population CAC > 0 was associated with higher all-cause mortality (pooled RR 3.23, 95% CI 2.12–4.93, P < 0.00001, I ² = 94%). In symptomatic population, revascularization in CAC > 0 was higher (pooled RR 15, 95% CI 6.66–33.80, P < 0.00001, I ² = 72) compared with CAC = 0. Additionally, CAC > 0 was associated with more revascularization in asymptomatic population (pooled RR 5.34, 95% CI 2.06–13.85, P = 0.0006, I ² = 93). In subgroup analysis of asymptomatic population by gender, CAC > 0 was associated with higher MACE (RR 6.39, 95% CI 3.39–12.84, P < 0.00001). Conclusion: Absence of CAC is associated with low risk of cardiovascular events compared with any CAC > 0 in both asymptomatic and symptomatic population without coronary artery disease.

Cardiac amyloidosis (CA) has emerged from the margins of cardiology to the forefront of research and practice on heart failure. Once regarded as rare and elusive, CA is now recognized as a significant cause of heart failure with preserved ejection fraction (HFpEF), arrhythmias, and valvular disease, especially in older patients. CA is characterized by extracellular deposition of misfolded protein fibrils, which infiltrate the myocardium and disrupt the structural and electrical integrity. Although CA can stem from multiple amyloid types, transthyretin amyloidosis (ATTR) and light-chain (AL) amyloidosis are the predominant subtypes with cardiac involvement, each carrying distinct implications for prognosis and therapy. This review explores CA as a clinical reality often obscured by more common cardiovascular syndromes. Moreover, this review focuses on the varied presentations of CA in real-world practice, how the condition overlaps with HFpEF, the subtle clues for CA amid common valvular disorders, and the complex rhythm manifestations of the condition. Particular attention is given to thromboembolic risk, microvascular dysfunction, and the evolving paradigm of preclinical or asymptomatic amyloidosis management. Furthermore, this review addresses contemporary challenges such as financial toxicity and the cost-effectiveness of screening, emphasizing the benefits of early detection and therapy. The paper also discusses risk stratification and staging, drawing from validated models to guide both prognosis and treatment decisions, and the role of histopathological characterization. Thus, this review underscores the importance of timely recognition and tailored intervention in transforming CA from a terminal diagnosis into a manageable chronic condition.

Background: The optimal anti-platelet regimen after transcatheter aortic valve replacement (TAVR) remains uncertain. The objective of this study was to compare the efficacy and safety of single anti-platelet therapy (SAPT) vs. dual anti-platelet therapy (DAPT) after transcatheter aortic valve replacement (TAVR). Methods: Electronic databases were searched for randomized and observational studies, which compared SAPT versus DAPT after TAVR. The primary outcomes were all-cause mortality, and major bleeding. Summary adjusted risk ratios (RR) were calculated using a Der-Simonian and Liard model. The risk of bias of the included studies was assessed by the Cochrane scale and New-castle Ottawa assessment tool. Results: A total of 10 studies with 2,412 patients were included. There was no difference in 30-days all-cause mortality (RR 1.19, 95% CI 0.79–1.81, p = 0.41, I² = 0.0%) and at the longest available follow up (i.e. mean 6.4 months) (RR 1.03, 95% CI 0.69–1.57, p = 0.86, I² = 0.0%). The risk of major bleeding was higher in the DAPT group (RR 2.14, 95% CI 1.37–3.31, p = 0.001). These findings were consistent on analyzing randomized versus observational studies (P_interaction = 0.97, and 0.76 for all-cause mortality and major bleeding, respectively). There was no difference in the risk of life-threatening bleeding, major vascular complications, myocardial infarction, and stroke between both groups (all p-values > 0.05). Conclusion: DAPT post TAVR is associated with an increased risk of major bleeding with no benefit on mortality, stroke, or myocardial infarction. The evidence is driven mainly from observational studies, and therefore future high quality randomized trials are needed.