Spontaneous coronary artery dissection (SCAD) has emerged as an important cause of acute coronary syndrome, myocardial infarction, and sudden death, particularly among young women and individuals with few conventional atherosclerotic risk factors. Patient-initiated research has spurred increased awareness of SCAD, and improved diagnostic capabilities and findings from large case series have led to changes in approaches to initial and long-term management and increasing evidence that SCAD not only is more common than previously believed but also must be evaluated and treated differently from atherosclerotic myocardial infarction. High rates of recurrent SCAD; its association with female sex, pregnancy, and physical and emotional stress triggers; and concurrent systemic arteriopathies, particularly fibromuscular dysplasia, highlight the differences in clinical characteristics of SCAD compared with atherosclerotic disease. Recent insights into the causes of, clinical course of, treatment options for, outcomes of, and associated conditions of SCAD and the many persistent knowledge gaps are presented.

Placental hypoperfusion may lead to an imbalance in proangiogenic and antiangiogenic factors, notably an increase in soluble fms-like tyrosine kinsase-1 (sFlt-1), thereby leading to endothelial dysfunction. Progress has been made in terms of determining the factors which lead to preeclampsia. Potential novel biomarkers for predicting preeclampsia risk have been identified through this research. Preeclampsia not only has important implications for the health during pregnancy but also for future cardiovascular risk. However, the exact mechanism by which it increases cardiovascular risk and the degree of risk it portends are yet to be elucidated.

Purpose of Review COVID-19 is now a global pandemic and the illness affects multiple organ systems, including the cardiovascular system. Long-term cardiovascular consequences of are not yet fully characterized. This review seeks to consolidate available data on long-term cardiovascular complications of COVID-19 infection. Recent Findings Acute cardiovascular complications of COVID-19 infection include myocarditis, pericarditis, acute coronary syndrome, heart failure, pulmonary hypertension, right ventricular dysfunction, and arrhythmia. Long-term follow-up shows increased incidence of arrhythmia, heart failure, acute coronary syndrome, right ventricular dysfunction, myocardial fibrosis, hypertension, and diabetes mellitus. There is increased mortality in COVID-19 patients after hospital discharge, and initial myocardial injury is associated with increased mortality. Summary Emerging data demonstrates increased incidence of cardiovascular illness and structural changes in recovered COVID-19 patients. Future research will be important in understanding the clinical significance of these structural abnormalities, and to determine the effect of vaccines on preventing long-term cardiovascular complications.

Background Spontaneous coronary artery dissection (SCAD) is a relatively rare cause of acute coronary syndrome historically thought to primarily affect young, healthy women. The lack of multicenter collaborative research efforts has made it challenging to identify the precise etiology and pathological mechanisms underlying SCAD. However, there are many similarities in the patient demographics, clinical presentations, and predisposing stressors between SCAD and takotsubo syndrome (TTS). Objectives The aim of this observational study was to examine the coronary and left ventriculographic features of patients with angiographically confirmed SCAD and determine the prevalence of concomitant TTS. Methods In this observational study, patients with angiographically confirmed SCAD were identified from the Massachusetts General Hospital SCAD registry. The coronary angiograms with simultaneous left ventriculograms (LVG) were carefully analyzed by an independent and blinded angiographic core laboratory. Results From our analysis of patients with SCAD who also underwent a LVG at time of coronary angiography, we identified a high prevalence of SCAD and concomitant TTS. Conclusions Therefore, we present TTS as a plausible mechanistic etiology for SCAD in some patients. In light of this finding as well as the many similarities between SCAD and TTS, clinicians should be vigilant about the potential concomitant presence of these two entities. Additional future investigations further exploring the clinical implications of the association between SCAD and TTS are warranted.