"Spice" (Synthetic Marijuana) Induced Acute Myocardial Infarction: A Case Series.

Marijuana is the most widely abused "recreational" substance in the United States, with highest prevalence in young adults. It is reported to cause ischemic strokes, hepatitis, anxiety, and psychosis. Although it is associated with dose dependent tachycardia and can lead to coronary vasospasm, it has not been directly related to acute myocardial infarction (AMI). Marijuana induced coronary vasospasm can result in endothelial denudation at the site of a vulnerable atherosclerotic plaque in response to hemodynamic stressors, potentially causing an AMI. Spice refers to herbal mixture with composition and effects similar to that of marijuana and therefore is referred to as "synthetic marijuana." Herein, we report 3 cases of spice induced ST-segment elevation myocardial infarction. All patients were relatively young and had few or absolutely no risk factors for cardiovascular disease. All patients underwent emergent coronary angiography, with two needing stent placement and the third requiring only aspiration thrombectomy. Our case series emphasizes the importance of suspecting and investigating synthetic marijuana use in low risk young adults presenting with AMI.

Ventricular volume overload alters cardiac output distribution in rats during exercise.

A rat model for chronic left ventricular volume overload (a-v fistula, 2 mo) was used to test the effects of acute exhaustive treadmill exercise (EX) (5 min, 70 ft/min, 0 degrees grade) on cardiocirculatory hemodynamics and cardiac output (CO) distribution during heart failure (HF). Control (C) and HF rats were studied at rest (R) and during the last minute of EX. Heart rate (HR), mean arterial pressure (MAP), and left ventricular end-diastolic (LVEDP) pressure were recorded and CO, blood flow (BF) to various regions, and total CO distribution were determined by the radioactive microsphere technique. In HF, biventricular hypertrophy and elevated LVEDP at R were correlated with an average shunt size equaling 37% of total CO. In both groups, CO and HR rose during EX with no change in MAP. Systemic CO in HF was reduced compared to C during both R and EX. BF to splanchnic, renal, cutaneous, and testicular circulations was compromised at R in HF, whereas only skeletal muscle BF was compromised in HF during EX. Data for CO distribution suggest that the major effect of HF during R was increased delivery to the coronary and the skeletal muscle beds at the expense of the cutaneous and renal beds, whereas %CO to the cerebral, hepatic, and gastrointestinal beds was spared. During EX, %CO to skeletal muscle beds in HF was attenuated compared to C, whereas that to the coronary bed was increased with no change in other regions.

Acute effects of arterio-venous shunt on cardiovascular hemodynamics in rat.

The cardiovascular effects of an acute high cardiac output state (Acute HCO) were determined in rats 24 h after opening an abdominal aorta-caval shunt equal to 50% of total cardiac output (CO). Heart rate (HR), left ventricular peak (LVP), end diastolic (LVEDP), and arterial (AP) pressures, CO, stroke volume (SV), total systemic and regional vascular resistance (VR), regional blood flow (BF) (radioactive microspheres), and tissue fluid content data were collected. In Acute HCO, AP and LVP were reduced while LVEDP was elevated, total CO was increased and total VR was decreased while systemic CO and VR were unchanged. In Acute HCO, HR did not change significantly and SV was significantly increased. Lung water in Acute HCO was significantly greater than control. Regional BF changes in Acute HCO include skeletal muscle reflex vasoconstriction and splanchnic and cerebral dilation. The results in conjunction with previous data on chronic HCO indicate that in the rat (1) increased lung water which is absent after cardiovascular compensation is an acute result of HCO, and (2) the acute phase of cardiac compensation to HCO occurs in the absence of a tachycardia response.

Chronic arteriovenous shunt: evaluation of a model for heart failure in rat.

A model for high output heart failure (HCO) was developed in male, Sprague-Dawley rats using an abdominal aortocaval shunt equal to 50% of total cardiac output (CO) with 2 mo of postsurgical recovery. The model was evaluated by analysis of hemodynamics, peripheral blood flows (BF) (radioactive microspheres), and plasma catecholamine levels as well as mass and fluid content of organs. In HCO, CO and left ventricular end-diastolic pressure were increased with significant left and right ventricular hypertrophy. Mean blood pressure (BP) was unchanged, but pulse BP was increased in HCO. BF to skeletal muscle, cutaneous, and some splanchnic regions was reduced to HCO, whereas BF to the cerebral, coronary, and renal beds was protected. Plasma epinephrine and norepinephrine levels were significantly elevated in HCO suggesting enhanced sympathetic as well as adrenal catecholamine release. Tissue analysis indicated altered circulatory status secondary to HCO in liver, kidney, spleen, and lung. The results indicate that this model will be a relevant tool for studies of the circulatory effects of heart failure.

Cardiovascular response to acute aquatic and treadmill exercise in the untrained rat.

The cardiovascular effects of acute aquatic (AE) and treadmill (TE) exercise were determined in untrained adult male Sprague-Dawley rats. Animals were exercised to exhaustion or for a maximum of 5 min with either exercise mode and data collected during the last minute of exercise were compared to preexercise rest data. Heart rate and cardiac output increased only with TE; arterial pressure remained stable during both protocols. Regional blood flow was determined by the radioactive microsphere technique. Coronary flow increased only with TE. Skeletal muscle flow, determined in six muscle groups, increased more with TE (97 to 587%) than with AE (-44 to 260%) (flow in the quadriceps group decreased during AE). Flow to the skin and splanchnic regions decreased; cerebral flow increased in both groups. Blood gas data suggest lactic acidosis and hyperventilation only with TE. These data indicate that 1) the cardiovascular effects of acute, exhaustive bouts of AE and TE in the rat are not comparable, and 2) the hemodynamic changes occurring with exhaustive TE in rat, as in man, involve a shunting of blood to the regions of demand and away from the nonessential circulations.