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Observational and trial data have revealed significant improvement in cardiogenic shock (CS) mortality due to acute myocardial infarction (AMI) after introducing early coronary revascularization. Less is known about CS mortality due to heart failure (HF), which is increasingly recognized as a distinct entity from AMI-CS.In this nationwide observational study, the CDC WONDER database was used to identify national trends in age-adjusted mortality rates (AAMR) due to CS (HF vs. AMI related) per 100,000 people aged 35-84. AAMR from AMI-CS decreased significantly from 1999 to 2009 (AAPC: -6.9% [95%CI -7.7, -6.1]) then stabilized from 2009 to 2020. By contrast, HF-CS associated AAMR rose steadily from 2009 to 2020 (AAPC: 13.3% [95%CI 11.4,15.2]). The mortality rate was almost twice as high in males compared to females in both AMI-CS and HF-CS throughout the study period. HF-CS mortality in the non-Hispanic Black population is increasing more quickly than that of the non-Hispanic White population (AAMR in 2020: 4.40 vs. 1.97 in 100,000). The AMI-CS mortality rate has been consistently higher in rural than urban areas (30% higher in 1999 and 28% higher in 2020).These trends highlight the fact that HF-CS and AMI-CS represent distinct clinical entities. While mortality associated with AMI-CS has primarily declined over the last two decades, the mortality related to HF-CS has increased significantly, particularly over the last decade, and is increasing rapidly among individuals younger than 65. Accordingly, a dramatic change in the demographics of CS patients in modern intensive care units is expected.

Despite novel technologies for treating shock patients, cardiogenic shock mortality remains high. Trends of cardiogenic shock associated with acute myocardial infarction (AMI) have previously been described, though little is known about cardiogenic shock resulting from other causes, which has progressively been documented as a distinct entity from AMI-cardiogenic shock. Herein, we review the evolving epidemiology, novel classification schema, and future perspectives of cardiogenic shock.While AMI or mechanical complications of AMI are the most common causes, the incidence of etiologies of cardiogenic shock not related to AMI, particularly acute on chronic heart failure, may be increasing, with a growing burden of noncoronary structural heart disease.Mortality in cardiogenic shock remains high. Overall, these findings highlight the need to address the lack of effective treatments in this field, particularly for cardiogenic shock caused by diseases other than AMI. Novel classification systems may facilitate cardiogenic shock research.

Introduction: Pulmonary veno-occlusive disease (PVOD) is a rare subtype of pulmonary arterial hypertension (PAH) caused by intimal fibrosis of the pulmonary venules and septal veins. While the hemodynamic profile is suggestive of pre-capillary pulmonary hypertension, vascular obstruction distal to the pulmonary capillary beds distinguishes PVOD from other forms of PAH. Case: A 29-year-old woman presented with progressive dyspnea and fatigue. She was tachycardic, hypotensive, and volume overloaded on exam. ECG was notable for right-axis deviation. TTE showed a dilated, hypokinetic RV and small LV with mild global hypokinesis and septal flattening throughout the cardiac cycle. A CTA chest excluded pulmonary embolism but showed diffuse centrilobular ground-glass opacities and lymphadenopathy which raised suspicion for PVOD. She underwent right heart catheterization with the following measurements (mmHg): RA 14, PA 99/56 (mean 71), PCWP 12, and CI 1.1 L/min/m 2 with PVR 28.1 WU. Following initiation of an epoprostenol infusion, she became increasingly hypoxemic with repeat CT chest demonstrating dramatic worsening of ground-glass opacities and vascular congestion. This response to a vasodilator challenge led to a clinical diagnosis of PVOD. She was urgently listed for and underwent bilateral lung transplantation. Explanted lung tissue subsequently confirmed the diagnosis. Conclusion: In most forms of PAH, vasodilators mitigate arteriolar narrowing and improve pulmonary blood flow, while in PVOD they exacerbate pulmonary capillary congestion due to increased arteriolar blood flow relative to the venous outflow due to fixed narrowing of the pulmonary venule network. Because lung biopsy is contraindicated in severe pulmonary hypertension, the clinician must recognize that worsening pulmonary edema in response to vasodilator challenge with normal PCWP is a critical clue pointing towards PVOD. Timely diagnosis is essential given the poor prognosis for this condition for which lung transplantation is the definitive treatment.

Ventricular septal defect (VSD) is a lethal complication of acute myocardial infarction (AMI) and is often associated with cardiogenic shock. The optimal form of percutaneous mechanical circulatory support (MCS) for AMI-VSD is unknown.We used a previously validated cardiovascular model to simulate AMI-VSD with parameters adjusted to replicate average hemodynamics reported in the literature, including a pulmonary-to-systemic blood flow ratio of 3.0. We then predicted effects of different types of percutaneous MCS (including intra-aortic balloon pumping, Impella, TandemHeart, and extracorporeal membrane oxygenation) on pressures and flows throughout the cardiovascular system. The simulation replicated all major hemodynamic parameters reported in the literature with AMI-VSD. Inotropes and vasopressors worsened left-to-right shunting, whereas vasodilators decreased shunting at the expense of worsening hypotension. All MCS devices increased forward blood flow and arterial pressure but other effects varied among devices. Impella 5.0 provided the greatest degree of pulmonary capillary wedge pressure reductions and decreased left-to-right shunting. Extracorporeal membrane oxygenation worsened pulmonary capillary wedge pressure and shunting, which could be improved by adding Impella or passive left ventricular vent. Pulmonary-to-systemic blood flow ratio could not be reduced below 2.0, and pulmonary flows remained high with all forms of MCS.Although no form of percutaneous MCS normalized hemodynamics in AMI-VSD, pulmonary capillary wedge pressure and shunting were worsened by extracorporeal membrane oxygenation and improved by Impella. Accordingly, based on hemodynamics alone, Impella provides the optimal form of support in AMI-VSD. However, other factors, including team experience, device availability, potential for tissue ingestion, and clinical characteristics, need to be considered when choosing a percutaneous MCS device for AMI-VSD.

Ventricular septal defect (VSD) is a life-threatening complication of myocardial infarction (MI). Mortality is highest if VSD repair occurs within seven days following MI. We report a case of post-MI VSD stabilized with peripheral veno-arterial extracorporeal membrane oxygenation (VA-ECMO) followed by patch repair and implantation of a durable left ventricular assist device (LVAD).