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Cardiovascular disease, particularly myocardial infarction, remains a major cause of morbidity and mortality among young individuals. Although myocardial infarctions have declined significantly in the general population, this decline has not been uniformly observed in younger cohorts. Young adults often have different risk factors, including a higher burden of tobacco use and substance abuse, and they are less likely to be treated with preventive therapies since they are often categorized as having low risk. This review examines the existing literature on myocardial infarction in young patients, with a focus on risk factors, therapeutic challenges, and opportunities for prevention.

Purpose of reviewCalcific aortic stenosis (CAVS) is the most common form of valvular heart disease in developed countries, increasing in prevalence with the aging population. Surgical or transcatheter aortic valve replacement is the only treatment available for CAVS. However, these interventions are typically reserved for severe symptomatic aortic stenosis (AS). The purpose of this review is to summarize the recent literature in uncovering the underlying pathophysiology of CAVS in the setting of lipoprotein (a) [Lp(a)] and emerging therapies targeting Lp(a) which may help halt disease progression in CAVS. Recent findingsPathophysiologic, epidemiological, and genetic studies over the past two decades have provided strong evidence that Lp(a) is an important mediator of calcific aortic valvular disease (CAVD). Studies suggest that Lp(a) is a key carrier of pro-calcifying oxidized phospholipids (OxPL). The metabolism of OxPL results in a pro-inflammatory state and subsequent valvular thickening and mineralization through pro-osteogenic signaling. The identification of Lp(a) as a causal mediator of CAVD has allowed for opportunities for emerging therapeutic agents which may slow the progression of CAVD (Fig. 1).

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