Figure 1.

Conceptual mechanistic model of the long-term impact of a sepsis incident on cardiovascular disease development. The figure presents the impact of a sepsis (early phase) on long-term (late phase) cardiovascular disease development in three domains: biologic sequelae due to sepsis (blue), pathophysiology of cardiovascular dysfunction (white) and examples of cardiovascular disease phenotypes (green). The magnitude of long-term cardiovascular disease risk is likely dependent on pre-sepsis health state and clinical or subclinical cardiovascular dysfunction/disease (pre-sepsis) and biological mechanisms and pathophysiologic changes during the episode of sepsis and recovery.

Dashed arrows demonstrate how late biologic sequelae (deteriorating processes initiated or accelerated by a sepsis incident) may lead to the late clinical phenotypic changes. Over time, persistent systemic inflammation, progressive mitochondrial dysfunction, formation of reactive oxygen species, reduced nitric oxide bioavailability and procoagulant activity (late phase biologic sequelae) may lead to dysfunctional cardiovascular remodeling, which contributes to the development/progression of cardiovascular disease. We also demonstrated potential interactions between cardiovascular diseases such as development of atrial fibrillation might contribute the development of stroke, myocardial infarction or heart failure.