Despite advances in percutaneous coronary interventions and their widespread use, mortality in patients presenting with acute myocardial infarction (MI) complicated by cardiogenic shock (CS) has remained very high, and treatment options are limited. Limited evidences exist, supporting many of the routinely used therapies in treating these patients. In the present article, we discuss CS complicating MI in general and an update on the currently available treatment options, including inotropes and vasopressor, coronary revascularization, mechanical circulatory support devices, mechanical complications, and long‐term outcomes.

The foramen ovale plays a vital role in sustaining life in-utero; however, a patent foramen ovale (PFO) after birth has been associated with pathologic sequelae in the systemic circulation including stroke/transient ischemic attack (TIA), migraine, high altitude pulmonary edema, decompression illness, platypnea-orthodeoxia syndrome (POS) and worsened severity of obstructive sleep apnea. Importantly, each of these conditions is most commonly observed among specific age groups: migraine in the 20 to 40s, stroke/TIA in the 30-50s and POS in patients >50 years of age. The common and central pathophysiologic mechanism in each of these conditions is PFO-mediated shunting of blood and its contents from the right to the left atrium. PFO-associated pathologies can therefore be divided into (1) paradoxical systemic embolization and (2) right to left shunting (RLS) of blood through the PFO. Missing in the extensive literature on these clinical syndromes are mechanistic explanations for the occurrence of RLS, including timing and the volume of blood shunted, the impact of age on RLS, and the specific anatomical pathway that blood takes from the venous system to the left atrium. Visualization of the flow pattern graphically illustrates the underlying RLS and provides a greater understanding of the critical flow dynamics that determine the frequency, volume, and pathway of flow. In the present review, we describe the important role of foramen ovale in in-utero physiology, flow visualization in patients with PFO, as well as contributing factors that work in concert with PFO to result in the diverse pathophysiological sequelae.

Patients with Fontan circulation are frail and experience multisystem dysfunction including impaired exercise capacity, low resting and exercise-augmented cardiac output, and progressive liver fibrosis. However, common underlying biochemical abnormalities or disease-specific biomarkers have not been well-described. We wish to investigate Fontan and their matched healthy subjects using a nontargeted, followed by targeted metabolomic analysis. Patients with Fontan circulation were compared to age- and sex-matched healthy controls with regard to body composition, markers of frailty, cardiopulmonary exercise testing, and resting and exercise-augmented hemodynamics. Subsequently, the study participants underwent a nontargeted metabolomics assessment, followed by targeted plasma bile acid (BA) analysis. Twenty Fontan patients (28.8 ± 9.8 years of age; 35% women) and 20 healthy controls (29.7 ± 6.0 years of age; 30% women) were enrolled. Fontan patients had significantly lower skeletal muscle mass, took longer to complete the 5 times sit-to-stand test; achieved lower %VO₂ max, and had lower resting and postexercise hemodynamic parameters. Nontargeted metabolomics assessment demonstrated elevated BAs, oxylipins, and leucine metabolites in Fontan patients. Total BA as well as 17 BA components were markedly elevated in the Fontan patients. Selective BAs were negatively associated with age, degree of frailty, cardiopulmonary function, and hemodynamic parameters. Elevated BAs are associated with worsening Fontan physiology. These findings warrant further exploration.