Treatment of acute myocardial infarction (AMI) has improved significantly in recent years, but many patients have adverse left ventricular (LV) remodeling, a maladaptive change associated with progressive heart failure. Although this change is usually associated with large infarcts, some patients with relatively small infarcts have adverse remodeling, whereas other patients with larger infarcts (who survive the first several days after AMI) do not. This paper reviews the relevant data supporting the hypothesis that individual differences in the intensity of the post-AMI inflammatory response, involving 1 or more inflammatory-modulating pathways, may contribute to adverse LV remodeling. It concludes by outlining how individual variations in the inflammatory response could provide important novel therapeutic targets and strategies.

Intravenously administered MSCs for acute myocardial infarction attenuate the progressive deterioration in LV function and adverse remodeling in mice with large infarcts, and in ischemic cardiomyopathy, they improve LV function, effects apparently modulated in part by systemic anti-inflammatory activities.

Despite a similar scaffold strut thickness, the Magmaris sirolimus-eluting bioabsorbable magnesium scaffold was significantly less thrombogenic compared with the Absorb bioresorbable vascular scaffold in an ex vivo porcine arteriovenous shunt model. Further studies are needed to determine whether the reduced thrombogenicity of Magmaris will result in reductions in major cardiovascular events.

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Background: Cocaine use disorder (CUD) is a common problem in the United States and worldwide. The mechanisms by which cocaine induces acute cardiovascular toxicity are various. When systemically absorbed through inhaled or intravenous routes, cocaine induces an acute rise in the heart rate (HR) and blood pressure (BP) leading to a significant increase in the cardiac output (CO) and myocardial oxygen demand. Subjects with chronic CUD represent a special population that has experienced long-term cocaine exposure, often without showing signs of cardiovascular disease. We herein present prospectively collected data on the acute hemodynamic effects of intravenous cocaine in a cohort of nontreatment-seeking individuals with CUD without cardiovascular disease. Methods and Results: Baseline physiologic data were collected while participants underwent infusion of escalating doses of cocaine (10, 20, and 40 mg administered over 2 minutes) at baseline and after receiving single-blind placebo treatment. Continuous noninvasive hemodynamic monitoring was performed throughout the infusion sessions using the ccNexfin finger cuffs (Edwards Lifesciences Corp, Irvine, CA). The recorded arterial BP tracings allowed for the measurement of beat-to-beat changes in HR, BP, stroke volume, CO, and systemic vascular resistance (SVR). None of the subjects experienced a treatment-related serious adverse event. Cocaine produced significant dose-dependent increases in median HR, BP, CO, and +dP/dt (a measure of cardiac contractility) and a significant dose-dependent reduction in median SVR. Conclusions: Intravenous cocaine in a cohort of otherwise healthy subjects with CUD produced dose-dependent increases in CO, largely explained by an increase in HR, accompanied by a dose-dependent decrease in SVR.

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Background Takotsubo (stress) cardiomyopathy is an acute reversible heart failure syndrome initially described in Japanese patients, but now well characterized in Caucasians patients in Europe or of European descent. An initial observation has suggested a lower incidence of Takotsubo in non-Caucasian subjects, particularly in the African-American (AA) population in the United States of America. The purpose of this study was to assess whether epidemiologic and clinical differences were present in Takotsubo in a large urban hospital in Virginia, USA. Methods We used an informatics-based system to query electronic health records (TriNetX, Cambridge, MA, USA) to search for cases of Takotsubo between 2010 and 2018 and a corresponding cohort of patients with non-ST segment elevation acute myocardial infarction (NSTEMI). We then performed a chart-level review of 160 cases and obtained additional clinical information including symptoms, risk factors, co-morbidities, and in-hospital outcomes. This retrospective study was approved by the Institutional Review Board of our institution. Results We identified 260 cases of Takotsubo and 6,270 of NSTEMI in the same time period (1:24, 4.2%). Being AA was associated with an odds ratio of Takotsubo versus NSTEMI of 0.38 [0.29–0.50] (P=0.0001). With further evaluation of patients with Takotsubo (N=160), AA (N=44, 27.2%) and Non-Hispanic Caucasian (C) (N=110, 67.9%) had no differences in age and sex. AA patients with Takotsubo however were more likely than C patients to be affected by type II diabetes mellitus (38.6% versus 14.5%, P=0.002, OR 3.70 [1.65–8.28]), have history of drug abuse (27.3% versus 9.1%, P=0.009, OR 3.75 [1.48–9.49]) and of cocaine use in particular (9.1% versus 0.9%, P=0.024, OR 11.0 [1.19–101.4]). The pattern of wall motion abnormality was not different between the 2 groups. AA patients presented with a lower ratio of brain natriuretic peptide (BNP) to troponin I (41.9 [12.7–258] pg./ml versus 281 [42–890] pg/ml, P=0.022). There was no significant difference of in-hospital mortality between the AA and C groups (9.1% versus 25%, respectively, OR 0.40 [0.13–1.24], P=0.11). Conclusions The incidence and clinical characteristics of Takotsubo (stress) cardiomyopathy appear to be different between African-American and Non-Hispanic Caucasian patients. African-American patients are more likely to have diabetes and illicit drug usage, but have a lower BNP/troponin I ratio. Both AA and Non-Hispanic Caucasian patients have similar in-hospital mortality.