Is positron emission tomography enough to rule out cardiac sarcoidosis? A case report.

BACKGROUND: Cardiac sarcoidosis (CS) is associated with poor prognosis, yet the clinical diagnosis is often challenging. Advanced cardiac imaging including cardiac magnetic resonance (CMR) and positron emission tomographic (PET) have emerged as useful modalities to diagnose CS. CASE SUMMARY: A 66-year-old woman presented with palpitations. A 24-h Holter monitor detected a high premature ventricular contraction burden of 25.6%. She underwent two transthoracic echocardiograms; both showed normal results. Stress perfusion CMR did not show any evidence of ischaemic aetiology; however, myocardial lesions detected by late gadolinium enhancement (LGE) imaging raised suspicion for CS. While there was no myocardial uptake of fluorodeoxyglucose (FDG) in subsequent cardiac PET, high FDG uptake was seen in hilar lymph nodes. Lymph node biopsy confirmed the diagnosis of sarcoidosis. DISCUSSION: Cardiac magnetic resonance and PET imaging are designed to evaluate different aspects CS pathophysiology. The characteristic LGE in the absence of increased FDG uptake suggested inactive CS with residual myocardial scarring.

Supracristal Ventricular Septal Defect Complicated by Formation of an Aorto-Right Ventricular Outflow Tract Fistula: A Rare Cause of Biventricular Enlargement.

Aorto-right ventricular outflow tract fistulas typically occur secondary to trauma, infective endocarditis, and sinus of Valsalva aneurysm rupture. We describe an unusual case of a spontaneous aorto-right ventricular outflow tract fistula in the absence of such findings, instead forming secondary to a complicating supracristal ventricular septal defect and leading to dilated cardiomyopathy.

Relationship of Stress Test Findings to Anatomic or Functional Extent of Coronary Artery Disease Assessed by Coronary Computed Tomography Angiography-Derived Fractional Flow Reserve.

BACKGROUND: In the United States, functional stress testing is the primary imaging modality for patients with stable symptoms suspected to represent coronary artery disease (CAD). Coronary computed tomography angiography (CTA) is excellent at identifying anatomic coronary artery disease (CAD). The application of computational fluid dynamics to coronary CTA allows fractional flow reserve (FFR) to be calculated noninvasively (FFRCT). The relationship of noninvasive stress testing to coronary CTA and FFRCT in real-world clinical practice has not been studied. METHODS: We evaluated 206 consecutive patients at Loyola University Chicago with suspected CAD who underwent noninvasive stress testing followed by coronary CTA and FFRCT when indicated. Patients were categorized by stress test results (positive, negative, indeterminate, and equivocal). Duke treadmill score (DTS), METS, exercise duration, and chest pain with exercise were analyzed. Lesions ≥ 50%stenosis were considered positive by coronary CTA. FFRCT < 0.80 was considered diagnostic of ischemia. RESULTS: Two hundred and six patients had paired noninvasive stress test and coronary CTA/FFRCT results. The median time from stress test to coronary CTA was 49 days. Average patient age was 60.3 years, and 42% were male. Of the 206 stress tests, 75% were exercise (70% echocardiographic, 26% nuclear, and 4% EKG). There were no associations of stress test results with CAD > 50% or FFRCT < 0.80 (p = 0.927 and p = 0.910, respectively). Of those with a positive stress test, only 30% (3/10) had CAD > 50% and only 50% (5/10) had FFRCT < 0.80. Chest pain with exercise did not correlate with CAD > 50% or FFRCT < 0.80 (p = 0.66 and p = 0.12, respectively). There were no significant correlations between METS, DTS, or exercise duration and FFRCT (r = 0.093, p = 0.274; r = 0.012, p = 0.883; and r = 0.034, p = 0.680; respectively). CONCLUSION: Noninvasive stress testing, functional capacity, chest pain with exercise, and DTS are not associated with anatomic or functional CAD using a diagnostic strategy of coronary CTA and FFRCT.

Recurrent ventricular tachycardia associated with lipomatous metaplasia of a myocardial scar.

Lipomatous metaplasia in chronic postmyocardial infarction scars is a common and underappreciated finding seen in histopathology and cardiac MRI. Evidence suggests that lipomatous metaplasia is capable of altering the electroconductivity of the myocardium leading to re-entry pathways that are implicated in the pathogenesis of postmyocardial infarction arrhythmogenesis. We report a case of a patient who presented with non-sustained ventricular tachycardia and was found to have lipomatous metaplasia of a prior myocardial infarct-related scar.

Pulmonary embolism response team implementation improves awareness and education among the house staff and faculty.

A subset of high-risk pulmonary embolism (PE) patients requires advanced therapy beyond anticoagulation. Significant variation in delivery of care has led institutions to standardize their approach by developing Pulmonary Embolism Response Team (PERT). We sought to assess the impact of PERT implementation on house staff and faculty education. After implementation of PERT, we employed a targeted educational intervention aimed to improve PERT awareness, familiarity with treatment options, role of echocardiogram and Doppler ultrasound, and knowledge of acute PE risk stratification tools. We conducted an anonymous survey among the house staff and faculty before and after intervention to assess the impact of PERT implementation on educational objectives among clinicians. Initial and follow up samples included 115 and 109 responses. The samples were well represented across the subspecialties and all levels of training, as well as junior and senior faculty. Following the educational campaign, awareness of the program increased (72.2-92.6%, p < 0.01). Proportion of clinicians with reported comfort level of managing PE increased (82.4-90.8%, p = 0.07). Proportion of clinicians with self-reported comfort with explaining all available treatment modalities to patients increased (49.1-67.9%, p = 0.005). Proportions of responders who correctly identified the role of echocardiography in risk stratification of patients with known PE increased (73.9-84.4%, p = 0.07). Accurate clinical risk stratification of acute PE increased (60.2-73.8%, p = 0.03). The implementation of a targeted educational program at a tertiary care center increased awareness of PERT among house staff and faculty and improved physician's accuracy of clinical risk stratification and comfort level with management of acute PE.

Interactive hemodynamic effects of dipeptidyl peptidase-IV inhibition and angiotensin-converting enzyme inhibition in humans.

Dipeptidyl peptidase-IV inhibitors improve glucose homeostasis in type 2 diabetics by inhibiting degradation of the incretin hormones. Dipeptidyl peptidase-IV inhibition also prevents the breakdown of the vasoconstrictor neuropeptide Y and, when angiotensin-converting enzyme (ACE) is inhibited, substance P. This study tested the hypothesis that dipeptidyl peptidase-IV inhibition would enhance the blood pressure response to acute ACE inhibition. Subjects with the metabolic syndrome were treated with 0 mg of enalapril (n=9), 5 mg of enalapril (n=8), or 10 mg enalapril (n=7) after treatment with sitagliptin (100 mg/day for 5 days and matching placebo for 5 days) in a randomized, cross-over fashion. Sitagliptin decreased serum dipeptidyl peptidase-IV activity (13.08±1.45 versus 30.28±1.76 nmol/mL/min during placebo; P≤0.001) and fasting blood glucose. Enalapril decreased ACE activity in a dose-dependent manner (P<0.001). Sitagliptin lowered blood pressure during enalapril (0 mg; P=0.02) and augmented the hypotensive response to 5 mg of enalapril (P=0.05). In contrast, sitagliptin attenuated the hypotensive response to 10 mg of enalapril (P=0.02). During sitagliptin, but not during placebo, 10 mg of enalapril significantly increased heart rate and plasma norepinephrine concentrations. There was no effect of 0 or 5 mg of enalapril on heart rate or norepinephrine after treatment with either sitagliptin or placebo. Sitagliptin enhanced the dose-dependent effect of enalapril on renal blood flow. In summary, sitagliptin lowers blood pressure during placebo or submaximal ACE inhibition; sitagliptin activates the sympathetic nervous system to diminish hypotension when ACE is maximally inhibited. This study provides the first evidence for an interactive hemodynamic effect of dipeptidyl peptidase-IV and ACE inhibition in humans.