Transradial coronary angioplasty and stent implantation in acute myocardial infarction: initial experience.

Transradial coronary angioplasty and stent implantation in have been associated with reduced complications, length of stay and hospital costs when compared to the transfemoral approach. Fourteen high-risk patients with acute myocardial infarction underwent transradial coronary angioplasty and stent placement. All diagnostic and interventional procedures were successfully completed using 6 French guide catheters and ACS Tristar stents (Guidant Corporation, Santa Clara, California) up to 4 mm in diameter. Thirteen patients received glycoprotein IIb/IIIa inhibitors. There were no procedural or access site complications. The mean length of stay was 3.5 days and the mean time interval from initial radial cannulation compared favorably with 14 acute myocardial infarction patients undergoing transfemoral angioplasty and stent placement. Transradial angioplasty in acute myocardial infarction appears to be a safe and feasible option. The procedure time is not increased in experienced hands, and the combination of rare access site complications and early ambulation may lead to decreased morbidity and lower costs. Transradial angioplasty in acute myocardial infarction may be an attractive option in thrombolytic therapy patients (facilitated percutaneous coronary intervention) or those who require aggressive anticoagulation or antiplatelet therapy.

Frequency of success and complications of coronary angioplasty of a stenosis at the ostium of a branch vessel.

The authors of this study hypothesized that percutaneous transluminal coronary angioplasty of a stenosis at the ostium of a branch vessel, whether isolated or associated with a bifurcation stenosis, was associated with reduced procedural success and increased in-hospital complications. One hundred six patients with 119 ostial branch stenoses were compared with 1,168 patients who underwent angioplasty of nonostial branch stenoses. An ostial branch stenosis was defined as a stenosis in the proximal 3 mm of a major branch vessel (diagonal [n = 58], posterior descending [n = 21], obtuse marginal [n = 34] and intermediate [n = 6]). The ostial branch stenosis was isolated in 61% of the patients and associated with a bifurcation stenosis in 39%. Despite a balloon to artery ratio of 1.05:1, angiographic success was 74% of ostial branch stenoses versus 91% of nonostial stenoses (p less than 0.01). Furthermore, angioplasty of ostial branch stenoses resulted in a complication rate of 13 versus 5% for angioplasty of nonostial branch stenoses (p less than 0.01). Therefore, angioplasty of ostial branch stenoses results in decreased procedural success and significant residual stenosis despite adequate balloon sizing, suggesting arterial elastic recoil and a significant increase in complications.

Influence of naloxone on response to acute cardiac tamponade in conscious dogs.

During progressive acute cardiac tamponade (CT) in conscious dogs, cardiac output (CO) falls continuously while arterial blood pressure (BP) is well maintained until an abruptly terminal decline. This response is primarily dependent on alpha-adrenergic mechanisms. During hemorrhagic shock, the opioid receptor blocker naloxone increases CO and BP and improves survival perhaps by reversing an opioid-induced cardiovascular depression. We produced 10 episodes of decompensated CT (DCT; 30% decline in BP) by intrapericardial saline infusion (20 ml/min) in five euvolemic conscious dogs. CT resulted in a decrease in CO and BP from base line (3.79 +/- 0.37 l/min and 89.6 +/- 5.2 mmHg, means +/- SE) to DCT (1.35 +/- 0.15 l/min and 57.5 +/- 3.1 mmHg; P less than 0.05). Naloxone (3 mg/kg iv) given at the onset of DCT resulted in a prompt sustained return of BP to base-line levels (P less than 0.05) with no change in CO. Four more animals were studied before and during naloxone (3 mg/kg iv then 0.3 mg.kg-1.min-1 iv). DCT occurred at a higher intrapericardial pressure (20.1 vs. 18.3 mmHg; P less than 0.025) if CT were induced during naloxone treatment than in its absence. Thus naloxone during DCT promptly reversed hypotension with no change in CO and, if present during induction of CT, naloxone allowed slightly higher levels of intrapericardial pressure to be tolerated. Further studies are needed to determine whether naloxone produced these effects solely by its actions on opioid receptors. This study suggests that the interaction between opioid and adrenergic influences plays a role in causing hypotension during CT.

Clinical application of percutaneous cardiopulmonary bypass for high risk coronary angioplasty.

Percutaneous cardiopulmonary bypass support was electively instituted prior to coronary angioplasty in 16 patients at high risk for hemodynamic collapse. In all cases the dilated artery supplied greater than 2/3 of the functioning myocardium. Eight patients had moderate LV dysfunction with ejection fraction 25-40%. Eight patients had an ejection fraction less than 20%. A 21 French cannula and a 17 French cannula were percutaneously inserted into the femoral vein and artery. Cardiopulmonary bypass support was instituted using a Bio-Medicus centrifugal pump just prior to coronary angioplasty at flow rates of 3.5-5 liters/minute. Thirteen patients had single vessel angioplasty and three patients had multivessel angioplasty. Complete loss of systolic function was observed in 9 (56%) patients. This finding when present confirms the absolute requirement for cardiopulmonary support. Technical success was achieved in all 16 patients (100%), clinical success was achieved in 14 patients (88%). Patient followup (mean 10 months) revealed 3 patients with class I-II angina and 10 patients were asymptomatic. There was one late death. In conclusion, percutaneous cardiopulmonary bypass support for carefully selected high risk patients may allow coronary angioplasty to be performed safely and effectively despite complete loss of systolic function during balloon inflation.

Increasing atrial pressure during cardiac tamponade does not elevate plasma levels of the peptide ANP in conscious dogs.

1. Factors influencing the release of atrial natriuretic peptide (ANP) are not well understood. We chose a conscious euvolaemic canine model of cardiac tamponade to investigate the roles played by atrial blood pressure, transmural atrial pressure, atrial size, and arginine vasopressin (AVP) on ANP release since during cardiac tamponade the atrial transmural pressure and size decrease as atrial pressure increases. The haemodynamic response to acute cardiac tamponade in conscious dogs differs from that in anaesthetized or convalescent animals. 2. Eighteen mongrel dogs were prepared for the chronic measurement of: ascending aortic blood flow (electromagnetic flowmeter); intrapericardial, right atrial and aortic blood pressures, and the evaluation of right atrial size (two-dimensional echocardiography). After the animals had recovered from surgery, data were collected during progressive cardiac tamponade induced by intrapericardial infusion of warmed saline (20 ml/min) to the point of haemodynamic decompensation. Decompensated cardiac tamponade (DCT) was defined as a decline in mean aortic blood pressure to 70% of the level present when the pericardial space was drained of fluid (baseline) and was produced in all animals within 25 min. Plasma ANP and AVP levels were measured at selected intervals. 3. Cardiac output decreased progressively as intrapericardial pressure, right atrial blood pressure and heart rate increased. Mean aortic blood pressure was well maintained until late in tamponade when it declined rapidly, while atrial transmural pressure and atrial size decreased continuously. These haemodynamic changes were associated with stable ANP plasma levels. There was no significant change in AVP plasma levels from the baseline level of 2.5 +/- 0.4 pg/ml until the point of DCT when they abruptly increased to 117 +/- 36.4 pg/ml. 4. The ability to increase ANP plasma levels was confirmed in a subgroup of animals by noting the response to AVP injection. Although the animals were able to increase plasma ANP levels in response to AVP injection (when intrapericardial pressure was normal) and the plasma AVP level was markedly increased late in tamponade, the time course of plasma AVP elevation could not explain why plasma ANP levels did not decrease as atrial transmural pressure and atrial size declined. 5. Thus, although atrial distention and not simply atrial blood pressure must play a dominant role in stimulating ANP release from the atria, decreased atrial size does not result in lowering of plasma ANP levels below baseline levels in this conscious euvolaemic canine model.

The effect of regional myocardial ischemia on Doppler echocardiographic indexes of left ventricular performance: influence of heart rate, aortic blood pressure, and the size of the ischemic zone.

Doppler echocardiographic indexes of ascending aortic blood flow velocity have been found to be an effective method of assessing changes in left ventricular performance induced by myocardial ischemia in both experimental animal preparations and in patients. In eight opened-chest anesthetized dogs, we investigated the influence of heart rate, aortic blood pressure, and size of the ischemic zone on Doppler indexes during regional myocardial ischemia. With control of mean aortic blood pressure and heart rate, transient coronary artery occlusion resulted in a statistically significant decline in peak velocity and mean velocity when as little as 24% of left ventricular myocardium was rendered ischemic. However, when heart rate and mean aortic blood pressure were not controlled, significant declines in peak velocity and mean velocity occurred only with simultaneous two-vessel occlusions involving greater than 47% of left ventricular myocardium. Although transient coronary artery occlusions generally produced no significant change in heart rate in the absence of atrial pacing, significant declines in aortic blood pressure were observed. We conclude that Doppler indexes of left ventricular performance obtained during myocardial ischemia are influenced not only by the extent of myocardium rendered ischemic, but also by changes in mean aortic blood pressure.

Mixed venous blood gases are superior to arterial blood gases in assessing acid-base status and oxygenation during acute cardiac tamponade in dogs.

Recent reports using anesthetized ventilator-dependent animal models, have suggested that in certain shock states, a disparity exists between arterial and mixed venous blood gases with regard to acid-base status and oxygenation. In a chronically instrumented unanesthetized canine model of acute cardiac tamponade breathing room air, we studied the effect of a graded decline in cardiac output on arterial and mixed venous pH, PCO2, and PO2. Cardiac tamponade resulted in a profound arterial respiratory alkalosis, whereas mixed venous pH, PCO2, and calculated serum bicarbonate levels remained relatively unchanged. As intrapericardial pressure increased and cardiac output declined, the difference between arterial and mixed venous PCO2 progressively increased. Further, whereas arterial oxygenation improved as cardiac output declined, mixed venous oxygenation steadily worsened. This disparity began early in cardiac tamponade (reductions in cardiac output of 20-40%) long before arterial blood pressure began to fall and progressively worsened as hemodynamic deterioration and lactic acidosis developed. Our findings are consistent with the hypothesis that a reduction in blood flow, resulting in decreased CO2 delivery to the lungs, is the primary mechanism responsible for the difference in pH and PCO2 observed between arterial and mixed venous blood. In this conscious, spontaneously breathing animal model, mixed venous blood gases thus are superior to arterial blood gases in assessing acid-base status and oxygenation, even early in acute cardiac tamponade when the decline in cardiac output is in the range of 20 to 40% and arterial blood pressure has not changed significantly.

Cocaine-associated myocardial ischemia. Review of clinical and angiographic findings.

The incidence of cocaine use is increasing in the United States among both adolescents and adults. Once thought to be a relatively safe street drug, cocaine has recently been implicated in 12 episodes of myocardial infarction. The case reports of these patients were retrospectively reviewed to determine the clinical and angiographic findings. All 12 patients exhibited electrocardiographic and angiographic evidence of myocardial infarction "shortly after" the use of cocaine by the nasal or intravenous routes. Most of the patients had fixed coronary artery disease. There appears to be increasing evidence of a temporal relationship between the use of cocaine and subsequent myocardial ischemic events in a subgroup of patients with or without fixed coronary artery stenosis. Physicians should inquire about cocaine use in patients with unexplained ischemic episodes since this may represent a potentially reversible factor in the later development of myocardial infarction.