The right radial approach for stenting of lesions in the right coronary artery with anomalous take-off from the left sinus of valsalva.

Angioplasty and stenting of lesions located in anomalous right coronary arteries arising from the left sinus of Valsalva is technically challenging. We suggest that the right radial artery provides a more direct approach that is particularly advantageous in such cases and include illustrative case reports.

Racial differences in performance of invasive cardiac procedures in a Department of Veterans Affairs Medical Center.

Racial differences have recently been described in hospital practice, most notably with regard to cardiac procedure utilization. To evaluate the possible reasons behind these differences, we analyzed statistics generated from a surgical referral conference at a large, tertiary care Veterans Affairs hospital between the years 1988 and 1996. In this setting, there is no financial incentive for physicians to recommend or perform invasive procedures, as all physicians are salaried employees of the Veterans Administration. Furthermore, all patients presented at conference have already had cardiac catheterization and are felt to be potential candidates for surgery or angioplasty. Cardiac therapeutic procedures (surgery or percutaneous transluminal coronary angioplasty) were recommended for 1075 of 1474 (72.9%) Caucasian patients and 207 of 322 (64.3%) African-American patients (odds ratio 1.497, 95% confidence interval 1.160 to 1.932, p = 0.0022). Of those patients presented with the option of an invasive procedure, 32 of 207 (15.4%) African-American patients and 89 of 1075 (8.3%) Caucasian patients refused any invasive procedure (odds ratio 2.026, 95% confidence interval 1.311 to 3.130, p = 0.0025). We conclude that reluctance by African-American patients to undergo invasive cardiac procedures may help explain observed disparities in race-related cardiac care.

Prognostic significance of spontaneous echo contrast in the thoracic aorta: relation with accelerated clinical progression of coronary artery disease.

OBJECTIVES: The purposes of this study were to identify the incidence of aortic smoke in an unselected cohort of patients and to determine the utility of this measurement as a clinical marker for future coronary events and long-term cardiac prognosis. BACKGROUND: Although spontaneous echo contrast detected within the cardiac chambers has been associated with an increased risk of thromboembolism, less is known about "smoke" within the thoracic aorta and its relation to progression of coronary artery disease. METHODS: We prospectively assessed 118 unselected, consecutive male patients (mean age 67 years, range 29 to 86) who underwent transesophageal echocardiography (TEE). The presence of aortic smoke was identified by swirling echodense shadows distinct from high gain artifact. A positive result required confirmation by two of three independent observers. RESULTS: Aortic smoke without dissection was found in 25 of the patients (21%). Indications for TEE, coronary risk factors, the incidence of reduced left ventricular ejection fraction and mitral insufficiency and known coronary artery disease severity collectively did not differ significantly at baseline between the groups with and without smoke. Follow-up averaged 20.4 months (range 18 to 24) and was 100% complete for mortality and 98% complete for morbidity. The presence of aortic smoke was an independent predictor of myocardial infarction (16.0% vs. 2.2%, p < 0.005) and cardiac death (20.0% vs. 1.1%, p < 0.0001). These statistics remained significant after covarying for age, ejection fraction < 50%, hypertension, diabetes, aortic dimension, the presence of an atheromatous plaque and smoke in the left atrium. CONCLUSIONS: Spontaneous echo contrast detected within the thoracic aorta by transesophageal echocardiography is a common and important clinical marker that is strongly associated with an increased risk for future myocardial infarction and cardiac mortality. Future studies will attempt to define the pathophysiology of this relation and assess whether aggressive revascularization strategies and antithrombotic therapy may aid in the reduction of this risk.

Long-term prognostic significance of dobutamine echocardiography in patients with suspected coronary artery disease: results of a 5-year follow-up study.

OBJECTIVES: This study sought to assess the long-term prognostic utility of dobutamine stress echocardiography in predicting fatal and nonfatal cardiac events. BACKGROUND: Although dobutamine stress echocardiography has improved sensitivity and specificity for detection of coronary artery disease, little is known of its predictive value for long-term cardiac events. Therefore, we followed up 120 consecutive patients who underwent dobutamine echocardiography for suspected coronary disease from March 1989 to August 1991. METHODS: All patients presenting for coronary angiography for chest pain were eligible for recruitment. Follow-up was 100% complete at 5 years (range 3.0 to 6.1). Cardiac events were defined as cardiac death or nonfatal myocardial infarction or the need for coronary revascularization (coronary angioplasty or bypass surgery). RESULTS: Positive (n = 78) and negative (n = 42) dobutamine test groups differed in their rates of coronary artery bypass graft surgery (37.2% vs. 9.5%, p < 0.001, respectively) and mortality. Of 26 total deaths, 22 occurred in the group with positive dobutamine test results (28% vs. 9.5%, p < 0.018); all 7 cardiac deaths occurred in this group as well (9% vs. 0%, p < 0.045). By multivariate regression analysis, positive results on dobutamine echocardiography remained independently predictive of future cardiac death after left ventricular ejection fraction and other clinical variables were accounted for. CONCLUSIONS: A positive finding on dobutamine echocardiography is an independent predictor of long-term cardiac mortality, whereas a negative finding confers a significantly reduced likelihood of cardiac death as much as 5 years from initial testing. We conclude that dobutamine stress echocardiography can be used to predict which patients with suspected coronary artery disease are at low risk for cardiac death and do not require concurrent nuclear or invasive testing.

Time course of lysophosphatidylcholine release from ischemic human myocardium parallels the time course of early ischemic ventricular arrhythmia.

BACKGROUND: We determined the kinetics of the release of lysophosphatidylcholine (LPC) into the coronary sinus of patients undergoing stress tests after coronary artery bypass grafting. The kinetics were consistent with a role for this amphiphile in the pathogenesis of ischemic ventricular arrhythmia, a major cause of sudden death. METHODS: Stress testing was initiated in the operating suite by pacing at a rate of 160 beats/min for 2 min. Ischemia was then induced by clamping the bypass grafts to the anterior wall for a maximal time of 4 min. RESULTS: The pacing procedure induced a prompt but reversible increase in coronary sinus LPC concentration from a baseline of 60.9 +/- 2.5 to 83.8 +/- 5.0 mumol/l via pacing alone, and a further increase to 101.8 +/- 6.7 mumol/l when the grafts were clamped for 2 min (P < 0.01). Six minutes after the cessation of pacing, LPC concentration returned to 67.5 +/- 4.4 mumol/l. CONCLUSIONS: These results demonstrate that severe myocardial ischemia is an agonist for rapid release of LPC from the myocardium. Kinetics of this release paralleled the time-course of early onset of electrophysiologic changes in isolated myocytes and perfused heart preparations in vitro. These results indicate that LPC may have an important role in the pathogenesis of ischemic ventricular arrhythmia in patients.

Dobutamine stress testing in the cardiac catheterization laboratory.

Dobutamine stress ventriculography is a safe test that appears to separate groups of patients with and without significant coronary artery stenoses. In this study, all 7 patients with significant coronary artery stenoses who reached a heart rate > or = 110 beats/min had a positive stress test, whereas 9 of 10 control patients had a negative stress test.

Beta adrenergic stimulation and blockade in cirrhosis: effects on azygos vein blood flow and portal hemodynamics.

It is unknown whether beta adrenergic stress has adverse hepatic hemodynamic effects. Therefore, the authors studied the hemodynamic effects of beta adrenergic stimulation and subsequent blockade in 10 patients with cirrhosis (6 Childs A, 3 Childs B, and 1 Childs C) with known or suspected portal hypertension. Free and wedged hepatic vein pressures, hepatic venous pressure gradient, heart rate, mean arterial pressure, cardiac output, and azygos vein blood flow were measured at rest and after isoproterenol infusion (mean dose = 7.3 micrograms/min: target heart rate = 150% to 200% of resting heart rate). Esmolol, an ultra-short-acting beta blocker, was then infused (dose titrated to return heart rate to baseline), and all measurements were repeated. Based on the results, the authors conclude that beta adrenergic stress provoked by isoproterenol infusion significantly increases azygos vein blood flow and hepatic venous pressure gradient. Beta blockade with esmolol reduces azygos vein blood flow and hepatic venous pressure gradient significantly below baseline.

Lysophosphatidylcholine accumulation in ischemic human myocardium.

Lysophosphatidylcholine accumulates in the coronary sinus during pacing-induced myocardial ischemia in humans. This amphiphile accelerates Ca++ flux leading to cell injury in cultured cardiac myocytes, but it is not known whether lysophosphatidylcholine accumulation is injurious to human myocardium. In this study, we measured lysophosphatidylcholine in normal human myocardium obtained during cardiac surgery and exposed to ischemic conditions in vitro. Total lysophosphatidylcholine concentration (sum of lysophosphatidylcholine remaining in tissue and lysophosphatidylcholine released into the buffer) increased from 0.73 +/- 0.08 nmol/mg protein at baseline to 1.83 +/- 0.45 nmol/mg protein after 5 minutes of ischemia (p < 0.001), and was associated with evidence of cell injury (26% depletion of tissue lactate dehydrogenase). Significant lysophosphatidylcholine release into the incubation buffer (0.41 +/- 0.11 nmol/mg protein) also occurred after 5 minutes of ischemia. In contrast, there was no lysophosphatidylcholine accumulation or release and no lactate dehydrogenase depletion in oxygenated and perfused controls. Attenuation of lysophosphatidylcholine accumulation by incubation with lysophospholipase did not prevent cell injury. Lysoplasmalogen was not detected in ischemic tissue. We conclude that lysophosphatidylcholine accumulation is a marker of myocardial ischemia in humans.

Mechanisms of ventricular arrhythmias in acute ischemia and reperfusion.

Coronary occlusion leading to nearly total absence of myocardial perfusion is the major cause of lethal ischemic arrhythmia in humans. In this setting, intracellular acidosis rapidly develops and leads to accelerated K+ efflux from the myocyte. Other metabolites, including lipid amphiphiles such as LPC, also rapidly accumulate in the ischemic zone. Elevated extracellular K+ and LPC cause membrane depolarization, which leads to slow conduction and increased refractoriness. These electrophysiologic changes contribute to the development of re-entrant rhythms, which predominate during early ischemia (phase 1a). Diffusion of extracellular K+ from the ischemic zone and release of endogenous catecholamines result in improvement in electrophysiologic parameters and are associated with a short arrhythmia-free interval, which occurs approximately 10 minutes after coronary occlusion. A second phase of arrhythmia (1b) then occurs and may be due in part to catecholamine-mediated triggered activity. Irreversible cell injury occurs 15 to 20 minutes after coronary occlusion and is associated with cell Ca++ overload, loss of gap junctions, and impaired cell coupling. This may lead to re-entrant arrhythmias. Reperfusion of ischemic myocardium leads to arrhythmia predominantly mediated by non re-entrant mechanisms. In humans, these reperfusion arrhythmias are usually relatively benign.

Percutaneous mitral valvuloplasty following surgical repair of sinus venosus atrial septal defect.

Mitral valvuloplasty performed 5 y after repair of a sinus venosus ASD was difficult because of a thickened septum, but resulted in improved mitral valve opening and did not lead to ASD. Thus, prior repair of a sinus venosus ASD may not be an absolute contraindication to mitral valvuloplasty.

Potentiation of the depressant effects of lysophosphatidylcholine on contractile properties of cultured cardiac myocytes by acidosis and superoxide radical.

Lysophosphatidylcholine (LPC) accumulates in the heart during myocardial ischemia. This amphiphile accelerates Ca++ flux in cardiac myocytes and may mediate ischemic cell injury. In the present study, we evaluated the effects of LPC on the contractility of cultured neonatal rat heart cells. We also investigated the interactions between LPC and other prominent features of the ischemic milieu, acidosis, and superoxide radical. A photo-optical technique was used to measure the maximum velocities of shortening and relaxation (dS/dt and dR/dt) of cultured cells superfused with 0.1 to 100 mumol/L LPC. LPC, at all concentrations, initially increased dS/dt. After 1 minute, however, dS/dt decreased in a concentration-dependent manner in cells superfused with greater than 20 mumol/L LPC. The effect of LPC on relaxation was also dependent on LPC concentration. dR/dt increased at less than 40 mumol/L LPC but decreased at greater than or equal to 60 mumol/L LPC. Acidosis markedly potentiated LPC-mediated depression in dS/dt and dR/dt. In contrast, superoxide dismutase entirely prevented LPC-mediated depression of contractility. We conclude that whereas brief exposure to LPC stimulates contractility, prolonged exposure to greater than 40 mumol/L LPC depresses dS/dt and dR/dt in cultured myocytes. The depressant effects of LPC on contractility are potentiated by acidosis and superoxide radical. We postulate that LPC accumulation in the myocardium contributes to ischemia-mediated contractile dysfunction.

Effects of lysophosphatidylcholine on cultured heart cells: correlation of rate of uptake and extent of accumulation with cell injury.

In this study we evaluated the effects of lysophosphatidylcholine, a possible mediator of ischemic damage, on cultured neonatal rat heart cells. The rate and duration of lysophosphatidylcholine accumulation was correlated with Ca++ uptake and cell injury. The rate of carbon 14-labeled lysophosphatidylcholine accumulation during superfusion of the cells by 10 to 100 mumol/L 14C-labeled lysophosphatidylcholine was proportional to the concentration of lysophosphatidylcholine in the perfusate. Rapid accumulation of lysophosphatidylcholine (0.235 nmol/mg protein per minute), which occurred during 10 minutes of exposure to 100 mumol/L lysophosphatidylcholine, resulted in Ca++ overload and cell lysis. In contrast, slow accumulation of lysophosphatidylcholine by myocytes, which occurred during prolonged (1 hour) exposure to a sublethal micellar concentration (80 mumol/L) or very prolonged exposure (6 hours) to a submicellar concentration of lysophosphatidylcholine (10 mumol/L) did not result in Ca++ overload or irreversible injury despite more total lysophosphatidylcholine accumulation than during a single 10-minute exposure to 100 mumol/L lysophosphatidylcholine (p less than 0.005). Repeated brief exposures (5 minutes) to 100 mumol/L lysophosphatidylcholine separated by 20-minute recovery intervals also resulted in more lysophosphatidylcholine accumulation than during the lethal 10-minute exposure to 100 mumol/L lysophosphatidylcholine but did not result in irreversible injury. We therefore conclude that cardiac myocytes can tolerate slow accumulation of lysophosphatidylcholine and that factors other than the quantity of lysophosphatidylcholine accumulating in cells are determinants of the degree of injury sustained from exposure to lysophosphatides.

Preservation of left ventricular function in patients with total occlusion of the left anterior descending coronary artery and wide-caliber distal vessel filling by collateral vasculature.

The segmental ventricular function of 76 patients with total occlusion of the left anterior descending coronary artery (LAD) was analyzed to establish the relationship between ventricular function and the presence and angiographic appearance of the collateral circulation. The relationship between function and collateral supply was found to be significant (P less than .01). The only angiographic feature of the collateral vasculature that was associated with preserved function was the caliber of the distal LAD. Wide-caliber vessels were more likely to be associated with preserved ventricular function than thin vessels (P less than .01). In contrast, both rapidly filling collateral arteries and slow filling vessels were associated with preserved ventricular function. Collateral supply maintenance was significantly associated with preserved ventricular function, even when the collaterals arose from stenotic coronary arteries. Furthermore, despite marked differences in ventricular function between the base and apex of the heart, there was a true relationship between preserved ventricular function and the presence of collateral vessels for all segments of the anterior wall. These findings may be relevant to clinical decision making and to proper interpretation of studies of ventricular function following LAD occlusion.

Plasma apoproteins and the severity of coronary artery disease.

Plasma levels of lipids, lipoproteins, and apoproteins in 281 patients undergoing cardiac catheterization were correlated with the incidence and severity of coronary artery disease (CAD) to determine if measurements of apoprotein levels are more predictive of the presence and severity of CAD than the corresponding levels of lipoprotein lipids. In 156 men with CAD among 194 men in the study the only variable other than age that correlated with the severity of CAD, defined by the number of lesions and percent stenosis, was the ratio of apoprotein AI to apoprotein B (r = .1908, p less than .03). The ratio of apoprotein AI to apoprotein B was a more accurate predictor of the severity of CAD than was the ratio of the corresponding high-density to low-density lipoprotein levels (coefficients of partial determination of .07 and .035; p less than .001 and p less than .07, respectively). Multivariate analysis confirmed the independent effect of the ratio of apoprotein AI to apoprotein B on the severity of CAD even after adjustments were made for lipid levels, age, presence of hypertension or diabetes, and therapy with beta-blockers or diuretics. Among men with total occlusion of a coronary artery apoprotein E and apoprotein B levels were significantly higher than in control subjects with a similar extent of CAD (p less than .03). The lipid profiles of the 37 women with CAD were very different from those of the men.(ABSTRACT TRUNCATED AT 250 WORDS)

Left main coronary artery spasm following percutaneous transluminal coronary angioplasty.

A patient with reversible spasm of the left main coronary artery occurring shortly after successful angioplasty of a mid-LAD lesion is reported. Prompt recognition of this rare entity may be life-saving.

Lysophosphatidyl choline potentiates Ca2+ accumulation in rat cardiac myocytes.

Lysophosphoglycerides are amphiphilic phospholipids that accumulate in ischemic myocardium and elicit electrophysiological alterations in normoxic Purkinje fibers and ventricular muscle that are analogous to alterations characteristic of ischemic tissue in vivo and that are compatible with altered sarcolemmal permeability to divalent cations. To assess directly the potential influence of lysophosphoglycerides on calcium transport, we characterized changes in the accumulation of 45Ca2+ by cultured cardiac myocytes exposed to selected concentrations of lysophosphatidyl choline (LPC). Perfusion for 10 min with 80 microM LPC augmented the amount of 45Ca2+ in myocytes compared with that in control cells (5.1 +/- 0.7 vs. 2.8 +/- 0.26 nmols Ca2+/mg protein, respectively; P less than 0.005) but did not alter total cell calcium content measured by atomic absorption spectrometry (11.6 +/- 1.0 nmols/mg protein), suggesting equivalent augmentation of bidirectional Ca2+ flux by LPC. In contrast, perfusion for 15 min with 100 microM LPC not only augmented 45Ca2+ accumulation but also increased total cellular Ca2+ content, as the quantity of 45Ca2+ accumulated reached 16.9 +/- 1.4 nmols/mg protein, a value substantially exceeding the normal total Ca2+ content (P less than 0.0025 compared with control cells). In contrast to results observed after only a 5-min exposure to 100 microM LPC, Ca2+ accumulation induced by 15 min of perfusion was not precluded by verapamil (10(-8)M), could not be reversed by perfusion without LPC, and was associated with complete cessation of beating, markedly altered morphology, and substantial depletion of cellular creatine kinase activity. Thus LPC may not only contribute to malignant ventricular dysrhythmias but also may potentiate ischemic injury by facilitating calcium ingress.