Percutaneous transluminal coronary angioplasty in acute ischemic syndromes

Acute myocardial ischemic syndromes are apparently related to the underlying pathophysiology leading to the clinical instability. Depending on the completeness and the duration of blood deprivation, different clinical syndromes result, such as sudden death, acute transmural infarction, nontransmural infarction, or unstable angina. Recent clinical, angiographic, and pathologic studies have emphasized the important pathophysiologic link between unstable angina, acute myocardial infarction, and early postinfarction angina. The term unstable angina is used for prolonged episodes of myocardial ischemia at rest in the absence of detectable myocardial necrosis. However, in the acute situation, when a patient presents with chest pain and electrocardiographic signs of ischemia, the distinction between unstable angina and myocardial infarction is often difficult. The uncertainty of outcome in a specific patient forces one to provide maximal treatment. The prime goal of any intervention in this situation must primarily be the preservation or early restoration of antegrade flow in the ischemia-related artery, in order to resolve myocardial ischemia and to prevent (further) myocardial necrosis, and so to improve both shortand long-term mortality and morbidity. Despite the latest substantial improvements in surgical techniques, cardioplegia, anaesthesia, and postoperative care, there is still no consensus as to the safety of surgery in the management of these subsets of patients. As an attractive alternative to coronary artery bypass surgery, percutaneous transluminal coronary angioplasty would logically play an important role in the management of patients with acute myocardial ischemic syndromes

Omineca Miner, January, 02, 1915

BACKGROUND AND AIMS: Immature platelet fraction (IPF) represents the quote of younger and larger sized circulating platelets, a potential marker of platelet reactivity and major cardiovascular events. We aimed to assess the relationship between IPF levels and the prevalence and extent of coronary artery disease (CAD) in patients undergoing coronary angiography. METHODS: A cohort of consecutive patients undergoing coronary angiography in a single centre were included. Significant CAD was defined as at least 1 vessel stenosis >50%, while severe CAD was defined as left main and/or three-vessel disease. IPF levels were measured at admission by routine blood cells count (A Sysmex XE-2100). RESULTS: We included 1789 patients, divided according to quartiles values of IPF. IPF levels were directly related to active smoke (p = 0.02), and non-acute coronary syndrome as indication to angiography (p < 0.001), higher levels of haemoglobin and uric acid (p < 0.001, respectively) and lower platelet count (p = 0.003). Angiographic features did not significantly differ according to quartiles values of IPF, but for a lower degree of TIMI flow in patients with a higher percentage of reticulated platelets (p = 0.01) and a higher rate of lesions involving bifurcations (p = 0.05). IPF levels did not affect the prevalence of CAD (77% vs. 82.2% vs. 79.1% vs. 75.6%, p = 0.34, adjusted OR [95% CI] = 0.93 [0.82-1.05], p = 0.22), nor of severe left main/three-vessel CAD (28.5% vs. 34.4% vs. 32.2% vs. 33.1%, p = 0.27; adjusted OR [95% CI] = 0.99 [0.90-1.1], p = 0.88). CONCLUSIONS: The present study shows that among patients undergoing coronary angiography, the immature platelet fraction (IPF) is not associated with the prevalence and extent of coronary artery disease, and, therefore, should not be overlooked as a marker of coronary atherosclerosis

Coronary vasodilatory action after a single dose of nicorandil

Coronary hemodynamics and vasodilatory effects on major epicardial arteries were investigated after a single dose of nicorandil in 22 patients undergoing cardiac catheterization for suspected coronary artery disease. Nicorandil, 20 mg, was administered sublingually to 11 consecutive patients and 40 mg to 11 others. Systemic blood pressure decreased significantly without affecting the heart rate. Coronary sinus blood flow did not change significantly. As the mean aortic pressure decreased significantly by 13% after 20 mg and 21% after 40 mg of nicorandil, the calculated coronary vascular resistance decreased but did not reach statistical significance. There was a decrease in myocardial oxygen consumption (-14% and -22%, respectively), and this was consistent with a significant decrease in the calculated pressure-rate product of 19% and 24%, respectively. A total of 103 selected coronary segments, including 17 stenotic segments, were analyzed quantitatively using a computer-assisted coronary angiography analysis system. After 20 or 40 mg of nicorandil, a significant increase of the mean diameter was observed in the proximal (+9% and +7%), midportion (+10% and +11%) and distal (+15% and +13%) parts of the left anterior descending coronary artery. Corresponding values for the proximal (+13% and +10%) and distal (+10% and +15%) segments of the circumflex artery were observed. An increase in the obstruction diameter was also observed in all but 3 of the analyzed stenotic segments. The results demonstrate that nicorandil, in the route and doses used, causes a significant vasodilation in the major epicardial coronary segments, including most stenotic segments, and decreases the myocardial oxygen demand with little effect on the resistance vessels

Coronary angioplasty early after diagnosis of unstable angina

Coronary angioplasty (PTCA) was performed early after diagnosis of unstable angina in 71 patients who responded favorably with initial pharmacologic treatment and who also had persistent exertional angina. The patients selected for PTCA had predominantly single-vessel disease and a normal or slightly abnormal left ventricular function. PTCA was successful in 87% (62/71) of the patients and unsuccessful in 13% (9/71). There were no deaths related to PTCA. The incidence of myocardial infarction during the procedure was 10% (seven of the 71 patients). Urgent bypass surgery was necessary in 11% (eight of 71 patients) of the patients. All patients were followed up for 12 months. There was one late death and one late nonfatal myocardial infarction. During 12 months of follow-up there was recurrence of angina pectoris in 25% of the patients (14/62). The restenosis rate was 25% (13/52) in the patients with an initial successful PTCA who underwent repeat angiography. Improved cardiac functional status after sustained successful PTCA was demonstrated by the normal exercise capacity on bicycle exercise testing and the absence of ischemia on thallium 201 scintigraphy studies in 70% of the patients. At the 1-year follow-up visit after attempted coronary angioplasty in all 71 patients, the total incidence of deaths was 1.5% (one patient), myocardial infarction 11% (eight patients), and the need for revascularization 25% (emergency surgery eight patients, late surgery three patients, and repeat PTCA seven patients); 91% (64 of 70 patients) were symptom free. It is concluded that PTCA in selected patients with unstable angina initially stabilized with medical treatment is an effective treatment with an acceptable complication rate and an excellent 1-year prognosis

Argatroban During Percutaneous Transluminal Coronary Angioplasty: Results of a Dose-Verification Study.

Background. Thrombin is a key enzyme in thrombogenesis. In animals, specific antithrombotic therapy at the time of coronary angioplasty reduced the incidence of subacute occlusion and inhibited the restenosis response. Argatroban is a highly selective synthetic thrombin antagonist that binds in a competitive manner. This is a report of a dose-verification study, assessing the safety and feasibility of intravenous Argatroban administration in patients undergoing percutaneous transluminal coronary angioplasty. Methods. Before angioplasty an intravenous bolus of 30 g/kg argatroban was administered, followed by a continuous infusion of 3.5 g/kg/min for 72 hours. Bolus injection was repeated, and the infusion rate was increased in order to achieve an activated coagulation time (ACT) of over 300 seconds. Following interim analysis, the bolus and initial infusion rate for the subsequent treatment groups was determined. Study endpoints were the occurrence of adverse events, coagulation tests, and qualitative angiogram reading. Patients were monitored by continuous 12-lead electrocardiographic recording over 24 hours, and underwent control angiography 18–24 hours following angioplasty. Results. Four treatment groups, comprised of 2, 8, 9, and 11 patients, respectively, were studied. The first two patients were excluded from analysis, since the initial dose was ineffective to attain an ACT-authorizing coronary angioplasty. The group with the highest dosage received a 250 g/kg intravenous bolus of argatroban, followed by a 4 hour infusion of 15 g/kg/min. At 4 hours the infusion rate was lowered to 3.8 g/kg/min and was continued for 68 hours without adjustment for catheter removal. The adverse event profile included myocardial infarction, aortocoronary bypass graft, bailout procedures, and repeat coronary angioplasty. Thrombin-time (TT), activated partial thromboplastin time (APTT), and prothrombin time (PT) were significantly related to argatroban plasma concentration, as demonstrated by regression analyses (R-square 0.64, 0.71, and 0.84, respectively). Prothrombin fragments 1 and 2 and thrombin-antithrombin III complex did not fit into a mathematical model, but showed slightly increased levels after reduction or cessation of the infusion rate. Conclusions. This dose-verification study, including 30 patients at four dose levels, indicated that argatroban infusion in coronary angioplasty patients can be administered safely, and results in an adequate and predictable level of anticoagulation

Acute effects of intravenous nisoldipine on left ventricular function and coronary hemodynamics

The hemodynamic effects of nisoldipine were investigated in 16 patients with suspected coronary artery disease who underwent routine cardiac catheterization. Nisoldipine was given intravenously in a dose of 6 micrograms/kg over 3 minutes and measurements made before and after drug administration during spontaneous and matched atrial paced heart rate. During sinus rhythm, nisoldipine produced a significant increase in heart rate (19%, p less than 10(-5]. Left ventricular systolic pressure decreased 28% (p less than 10(-6) and left ventricular end-diastolic pressure did not change significantly (5%, difference not significant). Coronary sinus and great cardiac vein blood flow increased by 21% (p less than 0.02) and 25% (p less than 0.005), respectively, after nisoldipine administration. Simultaneously, mean aortic pressure decreased 33% (p less than 10(-6]; consequently, the global and regional coronary vascular resistances decreased by 50% (p less than 10(-4]. The decreases in global (-8%) and regional (-4%) myocardial oxygen consumption did not reach statistical significance. A 6% (not significant) increase in end-diastolic volume and an 11% (p less than 0.002) decrease in end-systolic volume resulted in an increase of 21% in stroke volume (p less than 10(-4] with a consistent increase in ejection fraction (+16%, p less than 10(-5]. Total systemic vascular resistance was reduced by 30% (p less than 0.0002). During spontaneous heart rate and matched atrial pacing, the time constant of isovolumic relaxation as assessed by a biexponential model, was significantly shortened.(ABSTRACT TRUNCATED AT 250 WORDS

Coronary vasodilatory action of elgodipine in coronary artery disease

The effects of intravenous elgodipine, a new second-generation dihydropyridine calcium antagonist, on hemodynamics and coronary artery diameter were investigated in 15 patients undergoing cardiac catheterization for suspected coronary artery disease. Despite a significant decrease in systemic blood pressure, elgodipine infused at a rate of 1.5 micrograms/kg/min over a period of 10 minutes did not affect heart rate and left ventricular end-diastolic pressure. The contractile responses during isovolumic contraction showed a slight but significant increase in maximum velocity (56 +/- 10 to 60 +/- 10 seconds-1; p less than 0.005), whereas the time constant of early relaxation was shortened from 49 +/- 11 to 44 +/- 9 ms (p less than 0.05). Coronary sinus and great cardiac vein flow increased significantly by 15 and 26%, respectively. As mean aortic pressure decreased, a significant decrease in coronary sinus (-27%) and great cardiac vein (-28%) resistance was observed, while the calculated myocardial oxygen consumption remained unchanged. In all, 69 coronary segments (including 13 stenotic segments) were analyzed quantitatively using computer-assisted quantitative coronary angiography. A significant increase in mean coronary artery diameter (2.27 +/- 0.53 to 2.48 +/- 0.53 mm; p less than 0.000001), as well as in obstruction diameter, (1.08 +/- 0.29 to 1.36 +/- 0.32 mm; p less than 0.02), was observed. The results demonstrate that elgodipine, in the route and dose described, induces significant vasodilatation of both coronary resistance and epicardial conductance vessels, without adverse effects on heart rate, myocardial oxygen demand and contractile indexes