BACKGROUND:Acute myocardial infarction complicated by cardiogenic shock (AMI-CS) is the most common cause of mortality following AMI, and treatment algorithms vary widely. We report the results of an analysis using time-sensitive, hemodynamic goals in the treatment of AMI-CS in a single center study. METHODS:Consecutive patients with AMI-CS from November 2016 through December 2021 were included in our retrospective analysis. Clinical characteristics and outcomes were analyzed using the electronic medical records. We identified 63 total patients who were admitted to our center with AMI-CS, and we excluded patients who did not have clear timing of AMI onset or CS onset. We evaluated the rate of survival to hospital discharge based on the quantity of certain time-sensitive hemodynamic goals were met. RESULTS:We identified 63 patients who met criteria for AMI-CS, 39 (62%) of whom survived to hospital discharge. Odds of survival were closely related to the achievement of four time-dependent goals: cardiac power output (CPO) >0.6 Watts (W), pulmonary artery pulsatility index (PAPi) >1, lactate <4 mmol/L, and <2 vasopressors required. Of the 63 total patients, 36 (57%) received intra-aortic balloon pump (IABP) and 18 (29%) received an Impella CP (Abiomed) as an initial mechanical circulatory support strategy. Six patients were escalated from IABP to Impella CP for additional hemodynamic support. Nine patients were treated with vasopressors/inotropes alone. Regarding the 39 patients who survived to hospital discharge, 75% of patients met 3 or 4 goals at 24 h, whereas only 16% of deceased patients met 3 or 4 goals at 24 h. Of the 24 patients who did not survive to hospital discharge, 18 (75%) met either 0-1 goal at 24 h. There was no effect of the initial treatment strategy on achieving 3-4 goals at 24 h. CONCLUSION:Our study evaluated the association of meeting 4 time-sensitive goals (CPO >0.6 W, PAPi >1, <2 vasopressors, and lactate <4 mmol/L) at 24 h after treatment for AMI-CS with in-hospital mortality. Our data show, in line with previous data, that the higher number of goals met at 24 h was associated with improved in-hospital mortality regardless of treatment strategy.

Background Endomyocardial biopsy (EMB) remains the gold standard for cellular rejection surveillance in heart transplant recipients. Coronary artery fistula formation is a rare late and potentially catastrophic complication of repeated endomyocardial biopsies, without contemporary evidence on incidence or management. Case summary A 47-year-old male was found to have a fistula between his right ventricle and his left anterior descending artery on an angiogram that was performed as a part of regular screening of coronary allograft vasculopathy. Given the low shunt fraction, asymptomatic nature, and lack of guidelines on definitive management, the patient is undergoing conservative management with regular surveillance. Discussion Coronary artery fistulas were once thought to be rare complications of repeated EMB, but the true prevalence is likely to be higher than previously believed. Ideal treatment and monitoring is unknown given the relative rarity of the condition.

A 53-year-old man with a 3-year history of chronic cough was referred to us from another hospital. He had acute renal insufficiency, a nodular rash that had appeared 3 months previously (Fig. 1), and lower extremity edema. The patient also reported shortness of breath, weakness, and an unintentional weight loss of 15 lb. His vital signs were within normal limits. His breath sounds were coarse. No cardiac murmurs or rubs were audible. Nonblanching macules were seen on his right patella and dorsal right hand. Laboratory results included an elevated white blood cell count of 21.6 × 109/L with 46% eosinophils, a normal platelet count, an elevated serum creatinine level of 2.2 g/dL, and a hemoglobin level of 10.1 mg/dL. An electrocardiogram showed sinus rhythm. A transthoracic echocardiogram revealed a mobile echodensity in the right ventricle (RV) and mildly reduced left ventricular systolic function (Fig. 2A). On transesophageal echocardiograms, a 2.6 × 0.6-cm mass attached to the posterior aspect of the RV outflow tract (RVOT) had echogenicity similar to that of the myocardium (Fig. 2B), and a mobile 1.1 × 0.3-cm linear mass stemmed from the base of the anterior left ventricular endocardium, below the mitral valve annulus (Fig. 2C).Computed tomograms of the chest revealed bilateral ground-glass opacities. Bacterial and fungal blood cultures were negative. Histopathologic results of a kidney biopsy were consistent with antineutrophil cytoplasmic antibody–associated pauci-immune glomerulonephritis (Fig. 3). Our diagnosis was eosinophilic granulomatosis with polyangiitis (EGPA).We gave the patient cyclophosphamide and methylprednisolone, then discharged him from the hospital with prescribed prednisone. He decided to be monitored by doctors closer to his home and was lost to our follow-up.A rare systemic vasculitis, EGPA can present with various cardiac effects, including myopericarditis, arrhythmias, arteritis, and valvulopathies.1,2 Intracavitary thrombosis, as in this case, is rare. The leading theory is that eosinophilic infiltration of the myocardium mediates cardiac involvement.3 This case underscores the importance of performing echocardiography in patients with EGPA.

MicroRNAs (miRNA) are non-coding RNAs that regulate gene expression in up to 90% of the human genome through interactions with messenger RNA (mRNA). The expression of miRNAs varies and changes in diseased and healthy states, including all stages of myocardial ischemia-reperfusion and subsequent ischemia-reperfusion injury (IRI). These changes in expression make miRNAs an attractive potential therapeutic target. Herein, we review the differences in miRNA expression prior to ischemia (including remote ischemic conditioning and ischemic pre-conditioning), the changes during ischemia-reperfusion, and the changes in miRNA expression after IRI, with an emphasis on inflammatory and fibrotic pathways. Additionally, we review the effects of manipulating the levels of certain miRNAs on changes in infarct size, inflammation, remodeling, angiogenesis, and cardiac function after either ischemia-reperfusion or permanent coronary ligation. Levels of target miRNA can be increased using molecular mimics (“agomirs”), or can be decreased by using “antagomirs” which are antisense molecules that act to bind and thus inactivate the target miRNA sequence. Other non-coding RNAs, including long non-coding RNAs and circular RNAs, also regulate gene expression and have a role in the regulation of IRI pathways. We review the mechanisms and downstream effects of the miRNAs that have been studied as therapy in both permanent coronary ligation and ischemia-reperfusion models.