Ventricular Tachycardia Precipitated by the Use of the Diet Supplement Hydroxycut Gummies.

BACKGROUND: Dietary supplements have a long history of causing adverse effects. Ventricular arrhythmias have not been described with Hydroxycut Gummies. OBJECTIVE: To report a case of ventricular arrhythmia after prolonged use of a popular dietary supplement, Hydroxycut Gummies. CASE REPORT: An 18-year-old female with no significant past medical history presented with life-threatening ventricular arrhythmia following about 10 days of use of Hydroxycut Gummies, a legal dietary supplement previously unreported to cause this complication. The patient received external cardioversion due to progressive decline in mental status and persistent hypotension and was initiated on intravenous procainamide at an outside hospital. Left ventricular ejection fraction was 45% to 50%, and cardiac MRI showed no definite finding of infarct, myocarditis, or fibrosis. Beta-blocker therapy was initiated, and there was a progressive reduction in ventricular arrhythmia burden with an improvement of symptoms over the next few days. Two and a half months after the initial hospitalization, follow-up Holter monitor revealed occasional accelerated idioventricular rhythm events and a significant reduction in, but still occasional, long monomorphic ventricular tachycardia events. None of the ingredients listed in this product have been associated with cardiac dysrhythmias in the literature. One phytochemical potentially in the product is alpha-quinidine, which could be the cause of the adverse event. However, there was no other identifiable etiology for the ventricular tachycardia, which resolved after the discontinuation of supplement and the addition of beta-blocker therapy. CONCLUSION: Hydroxycut Gummies should be considered a probable cause of this patient's arrhythmia given the lack of another etiology and a Naranjo Scale score of 6.

Roof-dependent Atrial Flutter Changed into Single-loop Biatrial Flutter During Ablation.

A single-loop biatrial flutter is an uncommon form of atypical atrial flutter, and it can occur with septal or anterior line ablation in the left atrium (LA). We report a case with a roof-dependent atrial flutter that changed into a single-loop biatrial flutter during roof-line ablation. The activation entered the right atrium (RA) at the septum/fossa ovalis and coronary sinus ostium, exited the RA likely via the Bachmann's bundle and/or septopulmonary bundle, and entered the LA posterior to the roof line. The biatrial flutter was terminated with linear ablation between the right and left inferior pulmonary veins. RA mapping and biatrial flutter should be considered if roof-dependent atrial flutter slowed down during the roof-line ablation without termination.

Angiotensin II type 1 receptor blockade prevents alcoholic cardiomyopathy.

BACKGROUND: Activation of the renin-angiotensin system (RAS) may contribute to the development of alcoholic cardiomyopathy. We evaluated the effect of angiotensin II (Ang II) type 1 receptor (AT1) blockade on the development of alcoholic cardiomyopathy. METHODS AND RESULTS: We serially evaluated left ventricular (LV) and cardiomyocyte function and the RAS over 6 months in 3 groups of instrumented dogs. Eight animals received alcohol (once per day orally, providing 33% of total daily caloric intake); 6 received alcohol and irbesartan (5 mg.kg(-1).d(-1) PO); and 8 were controls. Compared with controls, alcohol ingestion caused sustained RAS activation with progressive increases in plasma levels of Ang II, renin activity, LV angiotensin-converting enzyme activity, and LV myocyte Ang II AT(1) receptor expression. The RAS activation was followed by a progressive fall in LV contractility (E(ES), alcohol-fed dogs 3.9+/-0.8 versus control dogs 8.1+/-1.0 mm Hg/mL); reductions in the peak velocity of myocyte shortening (78.9+/-5.1 versus 153.9+/-6.2 microm/s) and relengthening; and decreased peak systolic Ca2+ transient ([Ca2+]iT) and L-type Ca2+ current (I(Ca,L); P<0.05). Irbesartan prevented the alcohol-induced decreases in LV and myocyte contraction, relaxation, peak [Ca2+]iT, and I(Ca,L). With alcohol plus irbesartan, plasma Ang II, cardiac angiotensin-converting enzyme activity, and AT1 remained close to control values. CONCLUSIONS: Chronic alcohol consumption produces RAS activation followed by progressive cardiac dysfunction. The cardiac dysfunction is prevented by AT1 receptor blockade.

Growth hormone, insulin-like growth factor-1 and the aging cardiovascular system.

There is a large body of evidence that biological aging is related to a series of long-term catabolic processes resulting in decreased function and structural integrity of several physiological systems, among which is the cardiovascular system. These changes in the aging phenotype are correlated with a decline in the amplitude of pulsatile growth hormone secretion and the resulting decrease in plasma levels of its anabolic mediator, insulin like growth factor-1 (IGF-1). The relationship between growth hormone and biological aging is supported by studies demonstrating that growth hormone administration to old animals and humans raises plasma IGF-1 and results in increases in skeletal muscle and lean body mass, a decrease in adiposity, increased immune function, improvements in learning and memory, and increases in cardiovascular function. Since growth hormone and IGF-1 exert potent effects on the heart and vasculature, the relationship between age-related changes in cardiovascular function and the decline in growth hormone levels with age have become of interest. Among the age-related changes in the cardiovascular system are decreases in myocyte number, accumulation of fibrosis and collagen, decreases in stress-induced cardiac function through deterioration of the myocardial conduction system and beta-adrenergic receptor function, decreases in exercise capacity, vessel rarefaction, decreased arterial compliance and endothelial dysfunction leading to alterations in blood flow. Growth hormone has been found to exert potent effects on cardiovascular function in young animals and reverses many of the deficits in cardiovascular function in aged animals and humans. Nevertheless, it has been difficult to separate the effects of growth hormone deficiency from age-related diseases and associated pathologies. The development of novel animal models and additional research are required in order to elucidate the specific effects of growth hormone deficiency and assess its contribution to cardiovascular impairments and biological aging.

A Unique Case of Cardiac Arrest following K2 Abuse.

Sudden cardiac death (SCD) accounts for up to 450,000 deaths every year in the United States (Zipes et al. (2006)). Most cases of sudden cardiac death occur in subjects with no prior history of heart disease (Myerburg et al. (1998)). The incidence of sudden death in a general population has been shown to increase contemporaneously with substance abuse (Phillips et al. (1999)). The causative association of sudden death with cocaine, methadone, and volatile agents is well established (Adgey et al. (1995) and Isner et al. (1986)). We describe a case of out-of-hospital cardiac arrest temporally related to abuse of the synthetic cannabinoid street drug known as K2. To our knowledge, there are no previously documented cases of sudden cardiac death associated with synthetic cannabinoids although they have been linked to myocardial infarction in teenagers despite normal coronary angiography (Mir et al. (2011)).

Anomalous intracavitary right coronary artery shown by cardiac CT: a potential hazard to be aware of before various interventions.

Intracavitary right coronary arteries (RCAs) are uncommon (incidence of 0.09%-0.1%), having previously been reported nearly exclusively in autopsy series. However, more recently this entity has been detected prospectively by noninvasive cardiac computed tomography. Because many interventional procedures, including pacemaker placement and atrial flutter ablation, may be influenced by the presence of an intracavitary RCA, this entity is important to recognize. We report two cases of intracavitary right coronary artery discovered prospectively by cardiac computed tomography. In one of these cases, interventional management was altered based on our findings.

Enhanced inhibition of L-type Ca2+ current by beta3-adrenergic stimulation in failing rat heart.

beta3-adrenergic receptors (AR) have recently been identified in mammalian hearts and shown to be up-regulated in heart failure (HF). beta3-AR stimulation reduces inotropic response associated with an inhibition of L-type Ca2+ channels in normal hearts; however, the effects of beta3-AR activation on Ca2+ channel in HF remain unknown. We compared the effects of beta(3)-AR activation on L-type Ca2+ current (ICa,L) in isolated left ventricular myocytes obtained from normal and age-matched rats with isoproterenol (ISO)-induced HF (4 months after 340 mg/kg s.c. for 2 days). ICa,L was measured using whole-cell voltage clamp and perforated-patch recording techniques. In normal myocytes, superfusion of 4-[-[2-hydroxy-(3-chlorophenyl)ethylamino]propyl]phenoxyacetate (BRL-37,344; BRL), a beta3-AR agonist, caused a dose-dependent decrease in ICa,L with maximal inhibition (21%, 1.1 +/- 0.2 versus 1.4 +/- 0.1 nA) (p < 0.01) at 10(-7) M. In HF myocytes, the same concentration of BRL produced a proportionately greater inhibition (31%) in ICa,L (1.1 +/- 0.2 versus 1.6 +/- 0.2 nA) (p < 0.05). A similar inhibition of ICa,L was also observed with ISO (10(-7) M) in the presence of a beta1- and beta2-AR antagonist, nadolol (10(-5) M). Inhibition was abolished by the beta3-AR antagonist (S)-N-[4-[2-[[3-[3-(acetamidomethyl)phenoxy]-2-hydroxypropyl]amino]ethyl]phenyl]benzenesulfonamide (L-748,337; 10(-6) M), but not by nadolol. The inhibitory effect of BRL was attenuated by a nitric-oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (10(-4) M), and was prevented by the incubation of myocytes with pertussis toxin (PTX; 2 microg/ml, 36 degrees C, 6 h). In conclusion, beta3-AR activation inhibits L-type Ca2+ channel in both normal and HF myocytes. In HF, beta3-AR stimulation-induced inhibition of Ca2+ channel is enhanced. These effects are likely coupled with PTX-sensitive G-protein and partially mediated through a NOS-dependent pathway.