Diabetes, Heart Failure and Beyond: Elucidating the Cardioprotective Mechanisms of Sodium Glucose Cotransporter 2 (SGLT2) Inhibitors
Approximately 5 million individuals in the US are living with congestive heart failure (CHF), with 650,000 new cases being diagnosed every year. CHF has a multifactorial etiology, ranging from coronary artery disease, hypertension, valvular abnormalities and diabetes mellitus. Currently, guidelines by the American College of Cardiology advocate the use of angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, Î²-blockers, diuretics, aldosterone antagonists, and inotropes for the medical management of heart failure. The sodium glucose cotransporter 2 (SGLT2) inhibitors are a class of drug that have been widely used in the management of type 2 diabetes mellitus that work by inhibiting the reabsorption of glucose in the proximal convoluted tubule. Since the EMPA-REG OUTCOME trial, several studies have demonstrated the benefits of SGLT2 inhibitors in reducing cardiovascular risk related to heart failure. While the cardiovascular benefits could be explained by their ability to reduce weight, improve glycemic index and lower blood pressure, several recent trials have suggested that SGLT2 inhibitors exhibit pleiotropic effects that underlie their cardioprotective properties. These findings have led to an expansion in preclinical and clinical research aiming to understand the mechanisms by which SGLT2 inhibitors improve heart failure outcomes.
Exercise-Induced Sustained Ventricular Tachycardia without Structural Heart Disease: A Case Report
BACKGROUND Exercise-induced ventricular tachycardia (VT) has been widely reported in patients with preexisting structural heart disease or underlying ischemia and is attributed to reentry tachycardia and abnormal automaticity. However, studies regarding exercise-induced VT in individuals without evident structural heart disease are still limited. CASE REPORT A 51-year-old woman came to our practice for a treadmill stress echocardiogram. The patient experienced only mild chest discomfort and was otherwise asymptomatic. Cardiovascular risk factors were significant only for obesity and positive family history of coronary artery disease in the mother. During the exercise stress test, the patient developed wide complex VT with multiple capture beats accompanied by nausea and dizziness, which lasted approximately 2 minutes before resolving spontaneously. Subsequent evaluation with magnetic resonance imaging, transthoracic echocardiography, and coronary angiography revealed an absence of apparent structural heart disease. CONCLUSIONS Exercise-induced VT in the absence of structural heart disease, although rare, can pose a life-threatening event and requires different considerations for management. The benefits of currently available therapeutic options have yet to be elucidated for this subset of patients. Thus, we assert that there is a need for further investigation on the approach of exercise-induced VT in patients without structural heart disease.
A Late Case of Ischemic Cerebral Event after Resection of a Left Atrial Myxoma
Atrial myxoma is one of the most common primary cardiac tumors reported in the literature. In very rare instances, stroke has been the sequelae after a myxomatous tumor resection. We report this unique case of late ischemic cerebral event in a 46-year-old female some days after resection of a left atrial myxoma.
Effects of sildenafil on myocardial blood flow in humans with ischemic heart disease
BACKGROUND: We tested the hypothesis that sildenafil increases myocardial dilator reserve in humans with ischemic heart disease. METHODS: Positron emission tomography measured myocardial blood flow in 14 patients with ischemic heart disease. Patients were studied twice, in double-blind, placebo-control, cross-over design with sildenafil (or placebo) given approximately 2-3 h before measurements of hemodynamics and myocardial blood flow: at rest, with cold pressor stress and with adenosine. All myocardial segments of each patient with myocardial blood flow <1.65 ml/min per g with adenosine under placebo conditions were combined into one abnormal zone for that patient. Segments with myocardial blood flow >1.65 ml/min per g were averaged and combined into a normal zone for that patient. RESULTS: At rest, rate pressure product (heart rate x systolic arterial pressure, mmHg/min) was comparable, as was abnormal zone myocardial blood flow (ml/min per g; 0.76+/-0.48 placebo versus 0.64+/-0.20 sildenafil, both P=NS; mean+/-SD). Both rate pressure product and myocardial blood flow increased (P<0.01) with cold pressor stress (11+/-3 K and 1.14+/-0.59 placebo versus 10+/-3 K and 1.21+/-0.62 sildenafil). However, sildenafil failed to improve the myocardial blood flow response to cold pressor stress in abnormal or normal zones. In contrast, abnormal zone myocardial blood flow reserve with adenosine and sildenafil (2.6+/-0.7) exceeded that with adenosine and placebo (2.0+/-1.3, P<0.04, paired sign test). CONCLUSION: Sildenafil improves myocardial blood flow dilator response to adenosine in abnormal zones, possibly by augmenting nitric oxide-mediated increases in cGMP because adenosine response in part is nitric oxide dependent. Failure to improve myocardial blood flow response to cold pressor stress suggests that alpha-adrenergic constriction may offset enhanced nitric oxide effects. Clinically, the data suggest sildenafil may exert an anti-ischemic effect in patients with coronary artery disease.
Acute coronary syndrome critical pathway: chest PAIN caremap: a qualitative research study--provider-level intervention
Recently published data on healthcare performance continue to show a substantial gap between evidence-based guidelines and management of patients in real-world settings. This article describes an operational model that will be used to test whether a critical pathway applied in a secondary care-level institution may improve the process of care related to acute coronary syndromes (ACS). We have developed the pathway for management of all patients who present to our emergency department with a chief complaint of acute chest pain. Based on individual immediate ischemic event risk, patients are categorized according to a prespecified algorithm under the acronym of 'PAIN' (P-Priority risk, A-Advanced risk, I-Intermediate risk, and N-Negative/low risk) as prespecified in an algorithm. Along with the algorithm come 2 detailed order sets, 1 for ST-elevation ACS and another for non ST-elevation ACS. The pathway, together with the 2 order sets, are color-coded with the 'PAIN' acronym (P-red, A-yellow, I-yellow, N-green) that will guide patient management according to his or her risk stratification. These colors, similar to the road traffic light code, have been chosen as an easy reference for the provider about the sequential risk level of patients with ACS. This experimental model intends, with its unique structured approach, to increase awareness and improve adherence to the published American Heart Association/American College of Cardiology guidelines for the management of ACS