Novel distal occluder washout method for prevention of no-reflow during stenting of saphenous vein grafts.

This study assessed safety of the distal occlusion washout (DOW) method for prevention of no-reflow during stenting of degenerated saphenous vein grafts (SVGs). The DOW method involves protection of distal native coronary circulation with an occlusive balloon during the pretreatment and washout steps prior to stenting. Outcomes of stenting of 23 grafts in 21 patients after pretreatment with the DOW method were evaluated. The mean graft age was 7.4 +/- 4.3 years. The mean treated lesion length was 53 +/- 28 mm. Total occlusions were treated in 6 grafts and thrombotic lesions in 10 nontotally occluded grafts. One non-Q-wave MI and one acute stent thrombosis were observed. No deaths, Q-wave MIs, or subacute thromboses occurred. Follow-up in 18/21 (85.7%) patients at 28 +/- 8 weeks demonstrated target graft revascularization in 1 (5%) patient. The DOW method prevented clinically significant no-reflow in all 23 degenerated SVGs stented.

Effectiveness of aspirin and clopidogrel combination therapy in coronary stenting.

Two hundred fifty consecutive patients underwent coronary stenting and received a 2-week course of clopidogrel (75 mg orally each day after a loading dose of 150 mg) and aspirin. There was 1 (0.4%) in-hospital death, 1 (0.4%) acute stent thrombosis, and 2 (0.8%) subacute stent thromboses. There were no Q-wave myocardial infarctions, vascular complications, or repeat interventions at 30-day follow-up.

Exercise-induced secretion of atrial natriuretic factor and its relation to hemodynamic and sympathetic stimulation in untreated essential hypertension.

This study evaluates the release of atrial natriuretic factor (ANF) during maximal exercise in 7 patients with untreated moderate to severe hypertension with invasive monitoring of hemodynamic characteristics in relation to sympathetic activity. Peripheral venous ANF (fmol/ml) was determined at rest and maximal exercise producing a respiratory exchange ratio of 1.14 +/- 0.10. In 5 of 7 patients, simultaneous right ventricular and peripheral venous ANF samples could be obtained to assess exercise myocardial secretion of ANF. With exercise, mean blood pressure increased from 150 +/- 26 to 192 +/- 29 mm Hg (p less than 0.001), pulmonary wedge pressure increased from 7 +/- 3 to 18 +/- 10 mm Hg (p less than 0.05) and ANF increased from 11.7 +/- 8.2 to 25.7 +/- 15.9 (p less than 0.02). This ANF response correlated weakly with pulmonary wedge pressure (r = 0.497, p = not significant), since patients without an increase in pulmonary wedge pressure had no increase in ANF. However, changes in pulmonary wedge pressure and plasma norepinephrine during exercise were inversely correlated (r = -0.811, p less than 0.02), with the greatest increase in norepinephrine occurring with a minimal increase in pulmonary wedge pressure. Similarly, ANF and plasma norepinephrine were inversely correlated during exercise (r = -0.869, p less than 0.05). A significant increase in right ventricular ANF indicated myocardial secretion. Plasma ANF therefore increased because of active myocardial production during exercise in patients with moderate to severe hypertension. These findings further suggest a directionally opposing relation between ANF release resulting from increased atrial tension and sympathetic nervous system influence on cardiac performance during exercise.

Systemic and pulmonary hemodynamic responses to nicardipine during graded ergometric exercise in patients with moderate to severe essential hypertension.

In 10 patients with moderate to severe hypertension, the hemodynamic effects of ergometric exercise and nicardipine, a dihydropyridine calcium channel antagonist, were characterized under basal conditions and after 1 week of therapy. The responses of plasma renin activity and catecholamines were also assessed. Nicardipine induced significant reductions of systolic, diastolic and mean blood pressure under conditions of rest and peak exercise (p less than 0.001), mediated by reversal of vasoconstriction (p less than 0.001). Overall, cardiac index and stroke volume index responses were not significantly altered by nicardipine. Although rest pulmonary wedge pressure was unchanged (6 +/- 3 to 5 +/- 4 mm Hg), peak exercise pulmonary wedge pressure decreased from 24 +/- 22 to 7 +/- 5 mm Hg (p less than 0.001) with nicardipine therapy. This effect of nicardipine on pulmonary wedge pressure was present across all work loads studied, and was accompanied by reduction of peak exercise pulmonary artery pressure from 43 +/- 10 to 25 +/- 7 mm Hg (p less than 0.001). Oxygen consumption was unchanged, associated with reduction of arteriovenous oxygen difference (p less than 0.02). Both plasma renin activity (p less than 0.05) and norepinephrine (p less than 0.005) were significantly increased with nicardipine therapy. Thus, nicardipine produced significant blood pressure reduction by reversal of vasoconstriction in patients with essential hypertension. The preservation of cardiac output, with markedly reduced pulmonary wedge pressure, indicated that nicardipine improved ventricular performance in response to reversal of vasoconstriction.

Influence of baseline hemodynamic status and sympathetic activity on the response to nicardipine, a new dihydropyridine, in patients with hypertension or chronic congestive heart failure.

We evaluated the immediate hemodynamic response to nicardipine, administered as an intravenous bolus and 30-minute sustaining infusion, in 10 patients with systemic hypertension (HTN) and 10 patients with chronic congestive heart failure (CHF). Baseline systemic vascular resistance and the response to nicardipine for HTN (1968 +/- 657 to 905 +/- 256 dynes X sec X cm-5) and CHF (2002 +/- 988 to 1089 +/- 216 +/- 99 dynes X sec X cm-5) were virtually identical (P less than 0.01). In both groups there was a significant increase of cardiac index in response to afterload reduction: HTN, 2.70 +/- 0.46 to 4.47 +/- 1.01; CHF, 1.90 +/- 0.33 to 2.88 +/- 0.80 L/min/m2 (P less than 0.01), so that a negative inotropic effect was not evident. In HTN the increase in cardiac index was primarily the result of reflex increase of heart rate (67 +/- 16 to 95 +/- 25 bpm [P less than 0.05]), associated with norepinephrine increase from 402 +/- 243 to 744 +/- 364 pg/ml (P less than 0.001). In CHF the cardiac index increase was caused by a stroke volume index increase (23 +/- 4 to 33 +/- 9 ml/min; P less than 0.01), with no significant change in heart rate or norepinephrine. Thus nicardipine, by means of calcium channel antagonism, induced reversal of vasoconstriction. Differences in the cardiac response identify the importance of characterizing the pathophysiologic status of cardiac impairment to more accurately interpret pharmacologic interventions.

Atrial natriuretic factor in normal subjects and heart failure patients. Plasma levels and renal, hormonal, and hemodynamic responses to peptide infusion.

We investigated atrial natriuretic factor (ANF) in humans, measuring plasma immunoreactive (ir) ANF (in femtomoles per milliliter), and renal, hormonal, and hemodynamic responses to ANF infusion, in normal subjects (NL) and congestive heart failure patients (CHF). Plasma irANF was 11 +/- 0.9 fmol/ml in NL and 71 +/- 9.9 in CHF (P less than 0.01); the latter with twofold right ventricular increment (P less than 0.05). In NL, ANF infusion of 0.10 microgram/kg per min (40 pmol/kg per min) induced increases (P less than 0.05) of absolute (from 160 +/- 23 to 725 +/- 198 mueq/min) and fractional (1-4%) sodium excretion, urine flow rate (from 10 +/- 1.6 to 20 +/- 2.6 ml/min), osmolar (from 3.2 +/- 0.6 to 6.8 +/- 1.2 ml/min) and free water (from 6.8 +/- 1.6 to 13.6 +/- 1.6 ml/min) clearances, and filtration fraction (from 20 +/- 1 to 26 +/- 2%). Plasma renin and aldosterone decreased 33% and 40%, respectively (P less than 0.01). Systolic blood pressure fell (from 112 +/- 3 to 104 +/- 5 mmHg, P less than 0.05) in seated NL; but in supine NL, the only hemodynamic response was decreased pulmonary wedge pressure (from 11 +/- 1 to 7 +/- 1 mmHg, P less than 0.05). In CHF, ANF induced changes in aldosterone and pulmonary wedge pressure, cardiac index, and systemic vascular resistance (all P less than 0.05); however, responses of renin and renal excretion were attenuated. ANF infusion increased hematocrit and serum protein concentration by 5-7% in NL (P less than 0.05) but not in CHF.