Management of non-ST-Segment Elevation Myocardial Infarction.

Non-ST-segment elevation myocardial infarction (NSTEMI) is a major cause of cardiovascular morbidity and mortality in the United States. It represents the highest risk category of non-ST-segment elevation acute coronary syndromes (NSTEACS), for which timely diagnosis and appropriate therapy are paramount to improve outcomes. Evidence-based treatment, with combination of antiplatelet and anticoagulant therapy, and with serious consideration of early coronary angiography and revascularization along with anti-ischemic medical therapy, is the mainstay of management for NSTEMI. Aggressive risk-factor control after the acute event is imperative for secondary prevention of cardiovascular events. Applying in practice the American College of Cardiology/American Heart Association (ACC/AHA) guideline recommendations results in improved outcomes.

Acute and chronic reduction of functional mitral regurgitation in experimental heart failure by percutaneous mitral annuloplasty.

OBJECTIVES: We sought to determine acute and chronic efficacy of a percutaneous mitral annuloplasty (PMA) device in experimental heart failure (HF). Further, we evaluated the potential for adverse effects on left ventricular (LV) function and coronary perfusion. BACKGROUND: Reduction of mitral annular dimension with a PMA device in the coronary sinus may reduce functional mitral regurgitation (MR) in advanced HF. METHODS: Study 1: a PMA device was placed acutely in anesthetized open-chest dogs with rapid pacing-induced HF (n = 6) instrumented for pressure volume analysis. Study 2: in 12 anesthetized dogs with HF, fluoroscopic-guided PMA was performed, and dogs were followed for four weeks with continuing rapid pacing. RESULTS: Study 1: percutaneous mitral annuloplasty reduced annular dimension and severity of MR at baseline and with phenylephrine infusion to increase afterload (MR jet/left atrial [LA] area 26 +/- 1% to 7 +/- 2%, p < 0.05). Pressure volume analysis demonstrated no acute impairment of LV function. Study 2: no device was placed in two dogs because of prototype size limitations. Attempted PMA impaired coronary flow in three dogs. Percutaneous mitral annuloplasty (n = 7) acutely reduced MR (MR jet/LA area 43 +/- 4% to 8 +/- 5%, p < 0.0001), regurgitant volume (14.7 +/- 2.1 ml to 3.1 +/- 0.5 ml, p < 0.05), effective regurgitant orifice area (0.130 +/- 0.010 cm(2) to 0.040 +/- 0.003 cm(2), p < 0.05), and angiographic MR grade (2.8 +/- 0.3 device to 1.0 +/- 0.3 device, p < 0.001). In the conscious state, MR was reduced at four weeks after PMA (MR jet/LA area 33 +/- 3% HF baseline vs. 11 +/- 4% four weeks after device, p < 0.05) CONCLUSIONS: Percutaneous mitral annuloplasty results in acute and chronic reduction of functional MR in experimental HF.

Tachycardia during the valsalva maneuver: a sign of normal diastolic filling pressures.

Alteration of the loading conditions during the Valsalva maneuver is a helpful ancillary method in the noninvasive assessment of diastolic filling of the heart by Doppler echocardiography. When tachycardia is induced by the maneuver, mitral inflow velocity curves may become uninterpretable because of E velocity (the initial early diastolic velocity on the transmitral flow velocity curve) and A velocity (the velocity at atrial contraction on the transmitral flow velocity curve) wave fusion. To determine the clinical significance of the E velocity and A velocity wave fusion, our study assessed the relation between the heart rate response induced by the Valsalva maneuver and the left ventricular filling pressures measured during cardiac catheterization. In all, 77 patients performed the maneuver during continuous hemodynamic and electrocardiographic monitoring. The ratio between the baseline R-R interval and the shortest R-R interval during the maneuver was calculated. A ratio value higher than 1.1 was predictive of a pre-A pressure of less than 18 mm Hg (94% positive predictive value). Reflex tachycardia during the Valsalva maneuver and subsequent fusion of the E velocity and A velocity waves on the mitral velocity curves is a sign of normal left ventricular filling pressures.

Hemodynamic and humoral effects of vasopeptidase inhibition in canine hypertension.

Vasopeptidase inhibitors are potent new antihypertensive agents. The dual inhibition of ACE and neutral endopeptidase may result in synergistic humoral effects with unique hemodynamic actions. We investigated the hemodynamic and neurohumoral effects of vasopeptidase inhibition in conscious dogs made hypertensive by bilateral renal wrapping and subsequently instrumented for long-term assessment of left ventricular pressure and volume (n=8). Intravenous vasopeptidase inhibition (omapatrilat, 30 micromol/kg over 10 minutes) reduced peak left ventricular pressure (171+/-6 versus 130+/-6 mm Hg immediately after infusion, P<0.01) through arterial vasodilation (arterial elastance, 9.8+/-0.8 to 5.8+/-1.6 mm Hg/mL, P<0.01) and preload reduction (left ventricular end-diastolic volume, 51.1+/-6.8 to 46.0+/-6.9 mL, P<0.01). At 60 minutes, preload decreased further (40.5+/-5.9 mL, P<0.01 versus baseline). Vasopeptidase inhibition increased plasma levels of adrenomedullin (41.2+/-9.6 versus 72.3+/-15 pg/mL, P<0.01), whereas levels of the natriuretic peptides and cGMP were unchanged. Similar hemodynamic and humoral effects were observed with long-term therapy. Neither an equimolar dose of an ACE inhibitor (fosinopril) nor exogenous adrenomedullin had as potent of a hypotensive effect, and neither reduced preload. In summary, the potent short-term and long-term hypotensive effects of vasopeptidase inhibition were prominently mediated by preload reduction, an effect not reproduced by ACE inhibition nor adrenomedullin augmentation and not associated with enhanced natriuretic peptide levels. Combined arterial vasodilation and preload reduction may confer additional potency as well as unique cardioprotective effects. Synergistic effects on humoral and probably endothelial vasodilatory factors appear to be important in mediating the unique hemodynamic profile of vasopeptidase inhibition in this form of experimental hypertension.