Pheochromocytoma presenting as acute non-ST elevation myocardial infarction following elective hysterectomy.

INTRODUCTION: Studies have shown patients with pheochromocytoma have a 14-fold higher rate of cardiovascular events than patients with essential hypertension. CASE PRESENTATION: A 47-year-old female was found to have elevated troponins and marked ST depression following elective hysterectomy. The patient underwent cardiac catheterization, and labile blood pressures with a narrow-complex tachycardia were noted during the procedure. No evidence of coronary artery disease or wall motion abnormality was found. After catheterization, the patient complained of abdominal pain with difficulty passing gas. CT abdomen/pelvis revealed a 4.3 x 5 cm left adrenal mass. Plasma metanephrines and 24-hour urine catecholamines suggested pheochromocytoma. She underwent left total adrenalectomy, and pathology confirmed pheochromocytoma. At 3-month follow-up, she was asymptomatic and required only one agent for blood pressure control. DISCUSSION: Suspecting pheochromocytoma in patients with an unexpected myocardialevent and labile hypertension can lead to prompt diagnosis and appropriate preoperative management as well as avoidance of unnecessary procedures.

The ubiquitous mineralocorticoid receptor: clinical implications.

Mineralocorticoid receptors (MR) exist in many tissues, in which they mediate diverse functions crucial to normal physiology, including tissue repair and electrolyte and fluid homeostasis. However, inappropriate activation of MR within these tissues, and especially in the brain, causes hypertension and pathological vascular, cardiac, and renal remodeling. MR binds aldosterone, cortisol and corticosterone with equal affinity. In aldosterone-target cells, co-expression with the 11ß-hydroxysteroid dehydrogenase 2 (HSD2) allows aldosterone specifically to activate MR. Aldosterone levels are excessive in primary aldosteronism, but in conditions with increased oxidative stress, like CHF, obesity and diabetes, MR may also be inappropriately activated by glucocorticoids. Unlike thiazide diuretics, MR antagonists are diuretics that do not cause insulin resistance. Addition of MR antagonists to standard treatment for hypertension and cardiac or renal disease decreases end-organ pathology and sympathetic nerve activation (SNA), and increases quality of life indices.

Attenuation of oxidative stress and remodeling by cardiac inhibitor of metalloproteinase protein transfer.

BACKGROUND: Matrix metalloproteinase (MMP) and cardiac inhibitor of metalloproteinase (CIMP) are coexpressed in the heart. Although it is known that oxidative stress activates MMP and CIMP inhibits MMP, it is unclear whether CIMP administration attenuates oxidative stress and MMP-mediated cardiac dilatation. METHODS AND RESULTS: Arteriovenous fistula (AVF) was created in C57BL/J6 mice, and CIMP was administered to AVF and sham mice by protein transfer into peritoneal cavity by minipump for 4 weeks. Mice were grouped as follows: sham; sham+CIMP; AVF; and AVF+CIMP (n=6). In vivo left ventricular (LV) pressure was measured. Plasma and LV tissue levels of CIMP were measured by Western analysis. LV levels of NADPH oxidase activity, marker of oxidative stress, were increased in AVF mice and decreased in AVF mice treated with CIMP. Compared with sham, CIMP was decreased in AVF mice, and CIMP protein transfer increased plasma and LV tissue levels of CIMP in AVF mice; there was no increase in sham animals. In situ zymography demonstrated a robust increase in MMP activity in the hearts from AVF mice compared with sham, and treatment with CIMP decreased MMP activity. In AVF mice, the cardiac pressure-length relationship was similar to that observed in sham mice after administration of CIMP. Contractile responses of normal LV rings were measured in the presence and absence of CIMP. CIMP shifted the pressure-length relationship to the left, attenuated LV dilatation, and had no effect on CaCl2-mediated contraction. CONCLUSIONS: Treatment of AVF mice with CIMP significantly abrogated the contractile dysfunction and decreased the oxidative stress in volume overload-induced heart failure.