Coronary vasospasm while treating supraventricular tachycardia: is adenosine really to blame?

Coronary artery spasm has been reported during adenosine stress testing. Herein, we describe a transient ST-segment elevation following adenosine therapy for supraventricular tachycardia. A 38-year-old male presented to the emergency department with palpitations. Electrocardiogram showed supraventricular tachycardia with short RP interval. Vagal maneuvers were unsuccessful. Adenosine was then administered in two successive injections of 6 and 12 mg dosages, respectively. A subsequent 12-lead electrocardiogram revealed ST-segment elevation in inferior leads with reciprocal changes. Coronary angiography disclosed nonobstructive coronary disease. A postprocedure electrocardiogram exhibited normal sinus rhythm with nonspecific T wave abnormalities. Cardiac biomarkers were elevated with a peak troponin I of 0.32. Echocardiogram depicted bicuspid aortic valve and normal systolic function. Electrophysiological study revealed a concealed left accessory pathway and successful radiofrequency ablation was performed. Given the dynamic changes in the electrocardiogram, we hypothesize that this event was most likely a coronary vasospasm. The mechanism of coronary spasm following adenosine injection remains uncertain. Potential mediators include KATP channels and adenosine-2 receptors.

Pseudo-pulmonic stenosis in non-hodgkin's large B-cell lymphoma.

There have only been a few cases reported of right ventricular outflow tract obstruction secondary to diffuse large B-cell lymphomas. Mediastinal masses rarely cause extrinsic compression of the heart resulting in hemodynamically significant obstruction. We report a rare case of right ventricular outflow tract obstruction secondary to diffuse large B-cell lymphomas. Echocardiography has been found to be a useful modality in the prompt identification of mediastinal masses and their effects on the otherwise healthy heart.

Vasopeptidase inhibition with omapatrilat in chronic heart failure: acute and long-term hemodynamic and neurohumoral effects.

OBJECTIVES: We investigated the acute and long-term hemodynamic and neurohumoral effects of the vasopeptidase inhibitor omapatrilat in human heart failure. BACKGROUND: Angiotensin-converting enzyme (ACE) inhibition constitutes a major advance in the treatment of chronic heart failure (CHF). Simultaneous inhibition of both neutral endopeptidase and ACE with omapatrilat may represent a new treatment strategy in CHF. METHODS: Three hundred and sixty-nine patients with symptomatic heart failure were randomized to double-blind treatment with omapatrilat (first 190 patients: 2.5 mg, 5 mg or 10 mg; last 179 patients: 2.5 mg, 20 mg or 40 mg once daily) for 12 weeks. RESULTS: Acutely, the 10 mg, 20 mg and 40 mg doses of omapatrilat produced greater reductions in pulmonary capillary wedge pressure (PCWP), systolic blood pressure (SBP) and systemic vascular resistance compared with 2.5 mg. Higher doses were associated with greater increases in vasodilator and natriuretic peptides, in addition to ACE inhibition. After 12 weeks, omapatrilat 20 mg and 40 mg showed greater falls from baseline in PCWP (40 mg: 0 h to 12 h average change -7.3 +/- 0.8 mm Hg) and SBP (40 mg: -11.7 +/- 1.7 mm Hg) than 2.5 mg (both p < 0.01 vs. 2.5 mg). The incidence of adverse experiences and patient withdrawal were similar in all groups. CONCLUSIONS: In CHF, the acute hemodynamic benefit seen with higher doses of omapatrilat was associated with increases in plasma vasodilator and natriuretic peptide levels in addition to ACE inhibition. After 12 weeks, the hemodynamic benefit was maintained. Omapatrilat may be a promising new agent in CHF.