Effectiveness of the electronic medical record in cholesterol management in patients with coronary artery disease (Virtual Lipid Clinic).

This study demonstrates that the Virtual Lipid Clinic, an electronic medical record with computer-assisted cholesterol management, is associated with improved lipid management in patients with coronary artery disease. In comparison to traditional documentation methods with "pen and paper" charts, outpatient visits utilizing the electronic medical record were associated with a twofold increase in low-density lipoprotein (LDL) documentation, a threefold increase in achieving LDL goal, and a 30% increase in the use of lipid-lowering drugs.

Effect of platelet activation on coronary collateral blood flow.

BACKGROUND: The platelet products thromboxane A2 and serotonin have been shown to cause constriction of well-developed coronary collateral vessels. This study was performed to determine whether intravascular platelet activation produced with platelet activating factor (PAF) can cause a decrease in coronary collateral blood flow. METHODS AND RESULTS: Collateral vessel growth was induced by embolization of a hollow stainless steel plug into the left anterior descending coronary artery (LAD) of adult dogs. The animals were returned to the laboratory 3 to 6 weeks later for surgical instrumentation and measurement of collateral blood flow. Collateral flow was assessed by measuring retrograde blood flow from the cannulated collateral-dependent artery. PAF (10 nmol) was injected into the left main coronary artery to allow products of platelet activation to reach collateral vessels arising from the left coronary system. PAF caused a vasoconstrictor response, which became maximal 3 minutes after injection and resulted in a 40.3+/-7.4% decrease in retrograde blood flow (32.1+/-2.1 to 19.6+/-3.2 mL/min; P<0.05). By 15 minutes after the PAF injection, both retrograde blood flow and transcollateral resistance had returned to normal. After pretreatment with the thromboxane A2 receptor antagonist SQ30, 741, the vasoconstrictor response to PAF was abolished and, in contrast to the decrease in retrograde blood flow from PAF alone, a weak vasodilator effect was unmasked. CONCLUSIONS: PAF caused a decrease in coronary collateral blood flow. This vasoconstrictor response required the participation of thromboxane A2.

Nitric oxide inhibition impairs blood flow during exercise in hearts with a collateral-dependent myocardial region.

OBJECTIVES: We sought to determine the importance of nitric oxide (NO) production in maintaining coronary blood flow during exercise in hearts with collateral-dependent myocardium. BACKGROUND: Coronary collateral vessels demonstrate endothelium-mediated NO-dependent vasodilation in response to agonists such as acetylcholine. However, the contribution of endogenous NO production to maintaining vasodilation of coronary collateral vessels during exercise has not been previously studied. METHODS: Collateral vessel growth was induced in 13 chronically instrumented dogs by intermittent 2-min occlusions, followed by permanent occlusion of the left anterior descending coronary artery (LAD). One week after permanent LAD occlusion, myocardial blood flow was measured with microspheres during rest and treadmill exercise at 6.4 km/h at a 15% grade. Measurements were then repeated after blockade of NO production with N-nitro-L-arginine (LNNA) (20 mg/kg body weight intravenously). RESULTS: LNNA caused a 62 +/- 4% (mean +/- SEM) inhibition of the coronary vasodilation produced by acetylcholine. During rest conditions, LNNA caused a slight decrease in blood flow to the collateral region (p = NS), with no change in normal zone blood flow. During exercise, LNNA caused a decrease in mean blood flow to the collateral region (from 2.24 +/- 0.19 to 1.78 +/- 0.26 ml/min per g after LNNA, p < 0.05). This decrease resulted from a near doubling of the collateral vascular resistance (p < 0.05), with a trend toward an increase in small vessel resistance in the collateral zone. LNNA also reduced myocardial blood flow to the normal region during exercise (from 2.99 +/- 0.24 to 2.45 +/- 0.28 ml/min per g, p < 0.05) as the result of a 44 +/- 13% increase in coronary vascular resistance (p < 0.05). CONCLUSIONS: NO contributes to the maintenance of coronary collateral blood flow during exercise. In contrast to the normal heart, endogenous NO production also maintains blood flow in remote myocardial regions during exercise. These results suggest that control of blood flow during exercise in normal myocardium is altered by the presence of an occluded coronary artery.

Primary angioplasty reduces risk of myocardial rupture compared to thrombolysis for acute myocardial infarction.

Although the mechanical complications of acute ventricular septal defect and acute mitral regurgitation are uncommon after acute myocardial infarction, these complications are associated with an extremely high morbidity and mortality. We hypothesized that the administration of thrombolytic drugs may result in hemorrhagic infarction as well as the potential for incomplete revascularization and thus may lead to an increased incidence of mechanical complications compared to primary angioplasty. Accordingly, we reviewed the data of the most contemporary thrombolytic and primary angioplasty trials and compared the incidence of mechanical complications among 36,303 patients treated with thrombolytics reported in the GUSTO trial to the incidence of mechanical complications among 1,295 patients treated with primary angioplasty obtained from the PAMI-1 and PAMI-2 trials. We found that angioplasty resulted in an overall 86% relative risk reduction in mechanical complications (2.20% vs. 0.31%, P < 0.001). In comparison to thrombolytic therapy, angioplasty resulted in an 82% decrease in acute mitral regurgitation (1.73% vs. 0.31%, P < 0.001) and a 100% decrease in acute ventricular septal defect (0.47% vs. 0.00%, P < 0.03). In conclusion, in patients with acute myocardial infarction, reperfusion with primary angioplasty is associated with less myocardial rupture and mechanical complications than thrombolytics. This finding may, in part, explain the improved prognosis observed in myocardial infarction patients treated with primary angioplasty.

Treatment of no-reflow in degenerated saphenous vein graft interventions: comparison of intracoronary verapamil and nitroglycerin.

No-flow has been reported after 10-15% of percutaneous interventions on degenerated saphenous vein grafts. In this prospective study of 36 degenerated saphenous vein graft lesions (32 patients), no-flow (TIMI flow < 3 in the absence of a significant lesion or dissection) occurred in 15/36 (42%) lesions. A total of 32 episodes of no-flow occurred after angioscopy (n = 14), extraction atherectomy (n = 10), balloon angioplasty (n = 2) or stent implantation (n = 6). Intragraft nitroglycerin (100-300 micrograms) alone resulted in no improvement in TIMI flow in the setting of no-reflow (TIMI flow 1.2 +/- 0.6 to 1.4 +/- 0.8, P = NS). Intragraft verapamil (100-500 micrograms) resulted in improvement in flow in all 32 episodes (TIMI flow 1.4 +/- 0.8 before, to 2.8 +/- 0.5 after verapamil, P < 0.001). Although verapamil increased TIMI flow after all episodes of no-reflow, two (6.3%) had persistent no-reflow (TIMI 1) despite verapamil, associated with non-Q wave myocardial infarction. In conclusion, treatment of no-reflow with verapamil during degenerated vein graft interventions was associated with reestablishment of TIMI 3 flow in 88% of cases. In contrast, intragraft nitroglycerin alone was ineffective for reversing no-reflow.

Vasomotor responses of newly developed coronary collateral vessels.

Well-developed coronary collateral vessels contain an abundant muscular media and can undergo active vasomotion. However, early after coronary occlusion, coronary collateral vessels are thin walled with little smooth muscle, suggesting that vasomotor capability might be limited. Consequently, this study determined whether newly developed coronary collateral vessels have active vasomotor activity and whether endothelial function in these newly developed vessels is impaired. Retrograde blood flow was measured as an index of coronary collateral blood flow approximately 2 wk after embolic occlusion of the anterior descending coronary artery of dogs. Agonists were administered into the left main coronary artery to reach collaterals originating from the left coronary system. Baseline retrograde blood flow was 25.1 +/- 2.7 ml/min and increased to 36.7 +/- 3.7 ml/min after nitroglycerin (6 micrograms.kg-1.min-1, P < 0.05). Cyclooxygenase blockade with indomethacin (5 mg/kg i.v.) decreased retrograde collateral blood flow to 16.8 +/- 2.3 ml/min (P < 0.05). Subsequent administration of acetylcholine increased retrograde flow to 29.4 +/- 3.7 ml/min (P < 0.05), indicating intact endothelium-mediated vasodilation. Inhibition of nitric oxide synthase with NG-nitro-L-arginine further decreased coronary collateral retrograde flow to 12.0 +/- 2.8 ml/min (P < 0.05) and markedly blunted the response to acetylcholine. These findings demonstrate substantial vasomotor capability even early during coronary collateral development and indicate that both nitric oxide and cyclooxygenase-dependent endothelial mechanisms are intact.

Rapid hemodynamic improvement after reperfusion during right ventricular infarction.

OBJECTIVES: This study sought to determine the effects of reperfusion on hemodynamic status and hospital course in patients with right ventricular infarction. BACKGROUND: In contrast to the relatively low risk associated with acute inferior myocardial infarction, right ventricular infarction is associated with higher in-hospital morbidity and mortality. However, the potential benefits of reperfusion in patients with right ventricular infarction are unknown. Consequently, this study evaluated the potential benefits of primary angioplasty in patients with right ventricular infarction. METHODS: Of 141 consecutive patients admitted to the hospital for inferior myocardial infarction, 27 were identified as having right ventricular involvement by electrocardiographic and hemodynamic criteria. Seventeen patients achieved patency of the infarct-related right coronary artery by primary coronary angioplasty within 24 h of hospital admission, but 10 patients did not. All patients had invasive hemodynamic monitoring at the time of hospital admission, and subsequent serial hemodynamic status and clinical events were recorded. RESULTS: Patients with successful reperfusion demonstrated improved right atrial pressure, pulmonary capillary wedge pressure and right atrial/pulmonary capillary wedge pressure ratio as early as 8 h after reperfusion, whereas patients without reperfusion had no hemodynamic improvement over 24 h. Right atrial pressure demonstrated the greatest 8-h improvement after successful reperfusion (15.4 +/- 0.8 to 8.4 +/- 0.8 mm Hg [mean +/- SD], p < 0.05) but was unchanged without reperfusion (13.7 +/- 0.9 to 13.9 +/- 0.8 mm Hg, p = NS). Additionally, persistently elevated right atrial pressure was associated with increased mortality. CONCLUSIONS: Reperfusion in the setting of right ventricular infarction leads to rapid hemodynamic improvement and may result in improved survival.