Tachycardia-induced subendocardial necrosis in acutely instrumented dogs with fixed coronary stenosis.

UNLABELLED: It has been speculated but never proven that tachycardia-induced ischemia per se may lead to myocardial infarction. In 17 anesthetized dogs, the proximal left anterior descending (LAD) artery was cannulated and perfused via bypass from the left subclavian artery. Distal LAD pressure was reduced by a screw clamp to cause > or =20% decrease in wall thickening during pacing tachycardia but no decrease in resting heart rate (approximately 90 bpm). Dogs were randomly assigned to three groups: 1) control (n = 6) maintained at resting heart rate (approximately 90 bpm) and mean coronary pressure of 49+/-5 mm Hg for 4 h; 2) 4-h ischemia (n = 6), paced at 150 bpm and mean coronary pressure maintained at 59+/-6 mm Hg for 4 h; and 3) 1-h ischemia (n = 5), paced at 150 bpm and mean coronary pressure of 54+/-8 mm Hg for 1 h. Myocardial blood flow and infarct area were measured by radiolabeled microspheres and triphenyl-tetrazolium chloride staining, respectively. Despite the higher coronary pressure in the 4-h ischemia group (P = 0.02), patchy subendocardial necrosis occurred in all these dogs and in two of the 1-h ischemia dogs, and one control dog had minimal papillary muscle necrosis. Infarct area was largest in the 4-h ischemic group (15.5%+/-9.1%) compared with control and 1-h ischemia groups (0.09%+/-0.2% and 1.6%+/-2.1%, respectively) (P < 0.002). Relative (risk/ nonrisk areas) subendocardial flow was lower at the end of ischemia in the 4- and 1-h ischemia groups compared with the control group (0.3+/-0.1 and 0.4+/-0.1 vs 0.9+/-0.2; P = 0.008 and 0.01, respectively). Prolonged tachycardia-induced ischemia, in the face of fixed coronary stenosis causing no ischemia at the resting heart rate, leads to patchy subendocardial necrosis, despite anticoagulation and antiplatelet treatment. IMPLICATIONS: Prolonged tachycardia-induced ischemia, in the face of fixed coronary stenosis causing no ischemia at the resting heart rate, leads to subendocardial infarction in dogs. These findings suggest a possible mechanism for postoperative myocardial infarction.

Primary angioplasty in the treatment of acute myocardial infarction.

There are more than 600,000 acute myocardial infarctions (AMIs) in the United States each year, with direct medical costs exceeding $16 billion per year. Two treatment strategies are available for AMI today: medical therapy, including thrombolytic therapy, and primary angioplasty. Despite provocative preliminary data suggesting primary angioplasty results in lower mortality, morbidity and cost compared with thrombolytic therapy, most observers caution that more information is required before primary angioplasty replaces thrombolytic therapy for the treatment of AMI.

Exaggerated reactivity to mental stress is associated with exercise-induced myocardial ischemia in an asymptomatic high-risk population.

BACKGROUND: This study was done to determine whether cardiovascular reactivity to mental stress is associated with exercise-induced occult ischemia in an asymptomatic population at high risk for premature coronary heart disease (CHD). METHODS AND RESULTS: One hundred fifty-two siblings of persons with premature CHD underwent mental stress testing. Exercise thallium tomography and 24-hour Holter monitoring were also performed. Hemodynamic changes were monitored during both stressors. Siblings positive for exercise-induced ischemia were offered cardiac catheterization. During mental stress, siblings with an abnormal exercise ECG and/or thallium scan (n=15) had greater maximal increases in systolic blood pressure (SBP, P=.0004) and diastolic blood pressure (DBP, P=.05) and had greater heart rate variability in the normalized low frequency domain of an analysis of Holter monitor recordings, compared with siblings without exercise-induced ischemia. Coronary arteriography confirmed coronary atherosclerosis in 85% of siblings with exercise-induced ischemia. Regression analyses showed that occult ischemia during exercise was a strong independent predictor of maximal change in SBP and DBP during mental stress. A multivariate logistic model demonstrated that siblings with exercise-induced occult ischemia were 21 times more likely to be "hot" responders (top quartile of change in SBP and DBP) during mental stress. CONCLUSIONS: An exaggerated cardiovascular response to mental stress is associated with exercise-induced myocardial ischemia in persons with preclinical coronary heart disease.

Economic assessment of platelet glycoprotein IIb/IIIa inhibition for prevention of ischemic complications of high-risk coronary angioplasty. EPIC Investigators.

BACKGROUND: In the EPIC trial, c7E3 Fab, an antiplatelet IIb/ IIIa receptor antibody, reduced 30-day ischemic end points after high-risk coronary angioplasty by 35% and 6-month ischemic events by 23% but increased in-hospital bleeding episodes. METHODS AND RESULTS: Of the 2099 patients randomized in EPIC, data were collected on 2038 (97%) for prospective hospital cost and major resources. Physician fees were estimated from the Medicare Fee Schedule. Regression analysis was used to examine the economic tradeoff between reduced ischemic events and increased major bleeding during the initial hospitalization. A potential cost savings of $622 per patient during the initial hospitalization from reduced acute ischemic events with c7E3 Fab was offset by an equivalent rise ($521) in costs as the result of an increase in bleeding episodes. Baseline medical costs for the bolus and infusion c7E3 Fab arm averaged $13,577 (exclusive of drug cost) compared with $13,434 for placebo (P = .42). During the 6-month follow-up, c7E3 Fab decreased repeat hospitalization rates by 23% (P = .004) and repeat revascularization by 22% (P = .04), producing a mean $1270 savings per patient (exclusive of drug cost) (P = .018). With a cost of $1407 for the bolus and infusion c7E3 Fab regimen, the cumulative net 6-month cost to switch from standard care to routine c7E3 Fab averaged $293 per patient. CONCLUSIONS: In high-risk coronary angioplasty, aggressive platelet inhibition with c7E3 Fab, by significantly reducing ischemic events and repeat revascularization, recoups most of the cost of therapy and has the potential to pay for itself.

An anti-CD18 antibody limits infarct size and preserves left ventricular function in dogs with ischemia and 48-hour reperfusion.

OBJECTIVES: This study investigated whether an antibody against neutrophil adhesion protein CD18 could limit myocardial infarct size and preserve left ventricular function after prolonged reperfusion in a canine model. BACKGROUND: Myocardial reperfusion injury is mediated in part by accumulation of activated neutrophils. Although antibodies against CD18 have been shown to reduce neutrophil influx and infarct size after ischemia and 3 to 4 h of reperfusion, it is unknown whether protection is sustained beyond this time or whether there is meaningful preservation of ventricular function. METHODS: Dogs undergoing 90-min circumflex coronary artery occlusion and 48-h reperfusion were randomized to receive 1 mg/kg bodyweight of R15.7 (an anti-CD18 antibody, n = 12) or saline (control, n =12) 10 min before reperfusion. Contrast left ventriculography was used to measure left ventricular ejection fraction and regional chord shortening at baseline, during occlusion and at 48 h. Microspheres injected during occlusion were used to measure collateral flow and risk region size. Postmortem infarct size was measured with triphenyltetrazolium chloride. RESULTS: In the dose administered, R15.7 bound to neutrophils in vivo, with >85% saturation of CD18 for >24 h, with sustained antibody excess in the plasma. R15.7 significantly reduced infarct size after adjusting for the effect of collateral flow (p = 0.0002, analysis of covariance). In a subgroup of dogs with collateral flow <30% of nonischemic flow, infarct size was reduced from 34.6 +/- 3.9% (mean +/- SE) of the region at risk in the control group to 19.5 +/- 3.3% in the antibody group (p = 0.008). Ejection fraction and regional chord shortening did not differ between the two groups at baseline or during occlusion, but after 48-h reperfusion, ejection fraction and inferior wall regional cord shortening (representing the infarct zone) were both higher in the R15.7 group than the control group (43.6 +/- 2.9% vs. 28.5 +/- 1.8%, p < 0.01; 2.55 +/- 0.29% vs. 1.06 +/- 0.18%, p < 0.05). CONCLUSIONS: A single injection of an anti-CD18 antibody given before reperfusion can limit myocardial infarct size by nearly 50% and preserve global and regional left ventricular function after 48 h of reperfusion.

Coronary angioplasty, atherectomy and bypass surgery in cardiac transplant recipients.

OBJECTIVES: This study sought to analyze the outcomes of revascularization procedures in the treatment of allograft coronary disease. BACKGROUND: Allograft vasculopathy is the main factor limiting survival of heart transplant recipients. Because no medical therapy prevents allograft atherosclerosis, and retransplantation is associated with suboptimal allograft survival, palliative coronary revascularization has been attempted. METHODS: Thirteen medical centers retrospectively analyzed their complete experience with percutaneous transluminal coronary angioplasty, directional coronary atherectomy and coronary bypass graft surgery in allograft coronary disease. RESULTS: Sixty-six patients underwent coronary angioplasty. Angiographic success (< or = 50% residual stenosis) occurred in 153 (94%) of 162 lesions. Forty patients (61%) are alive without retransplantation at 19 +/- 14 (mean +/- SD) months after angioplasty. The consequences of failed revascularization were severe. Two patients sustained periprocedural myocardial infarction and died. Angiographic restenosis occurred in 42 (55%) of 76 lesions at 8 +/- 5 months after angioplasty. Angiographic distal arteriopathy adversely affected allograft survival. Eleven patients underwent directional coronary atherectomy. Angiographic success occurred in 9 (82%) of 11 lesions. Two periprocedural deaths occurred. Nine patients are alive without transplantation at 7 +/- 4 months after atherectomy. Bypass graft surgery was performed in 12 patients. Four patients died perioperatively. Seven patients are alive without retransplantation at 9 +/- 7 months after operation. CONCLUSIONS: Coronary revascularization may be an effective palliative therapy in suitable cardiac transplant recipients. Angioplasty has an acceptable survival in patients without angiographic distal arteriopathy. Because few patients underwent atherectomy and coronary bypass surgery, assessment of these procedures is limited. Angiographic distal arteriopathy is associated with decreased allograft survival in patients requiring revascularization.

A chimeric IgG4 monoclonal antibody directed against CD18 reduces infarct size in a primate model of myocardial ischemia and reperfusion.

OBJECTIVES: This study attempted to determine whether neutrophil sequestration in reperfused myocardium can be inhibited and infarct size reduced by treatment with a chimeric, monoclonal IgG4 antibody (CLB54) directed against CD18 in a primate model of acute myocardial ischemia and reperfusion. BACKGROUND: Reperfusion injury, in part mediated by neutrophils, may limit the potential benefit of reestablishing infarct-related artery patency in patients with acute myocardial infarction. METHODS: Nineteen closed-chest baboons (10 control, 9 treated with CLB54) had the left anterior descending coronary artery occluded for 90 min, followed by 4 h of reflow. CLB54 (mean [+/- SD] 11 +/- 2 mg/kg body weight) or saline solution was administered intravenously 20 min before reflow. Coronary flow was determined using radiolabeled microspheres, infarct size by triphenyltetrazolium chloride staining, global and regional ventricular function by contrast ventriculography and neutrophil accumulation by a myeloperoxidase assay. RESULTS: Risk region size was the same in both groups. CLB54 treatment reduced infarct size expressed as a percent of the risk region from 41 +/- 20% in the saline-treated group to 19 +/- 17% in the CLB54-treated group (p < 0.02). This was associated with diminished myeloperoxidase activity and greater postreperfusion coronary flow in the risk region in CLB54-treated than in control baboons. Ejection fraction declined to the same extent in both groups, whereas anterior wall regional cord shortening was better preserved in CLB54-treated baboons. CONCLUSIONS: Inhibition of neutrophil sequestration with CLB54 administered before reperfusion reduces infarct size, preserves ischemic zone microvascular perfusion and minimizes the decline of regional wall motion.

Analysis of high-frequency signal-averaged ECG measurements.

Analysis of high frequency (150-250 Hz) in the signal-averaged electrocardiogram (SAECG) is one of the emerging methods for detecting vessel patency in acute myocardial infarction following thrombolytic therapy and angioplasty. Root-mean-square voltage (RMSV) of the filtered QRS has been used in earlier studies to detect reperfusion; however, previous analysis indicated that RMSV is sensitive to residual noise in the SAECG and errors in QRS delineation (onset/offset). A new measurement is proposed, high-frequency energy (HFQE), and the robustness of the RMSV and HFQE was evaluated for simulated errors in QRS delineation. In this study, two measures (RMSV and HFQE) were tested on 24 control subjects and 21 patients undergoing thrombolytic therapy. Results indicate that unfiltered QRS duration is more stable than filtered QRS duration for the control subjects and patients and that HFQE had less fluctuation than RMSV in thrombolytic therapy patients. In the control group, HFQE was sensitive to the amplitude variation of the filtered SAECG. Therefore, another new measurement is proposed high-frequency integral of absolute value (HFAV), for reducing the sensitivity to amplitude changes in the filtered SAECG. This new feature was tested on control subjects and was found to be more stable than HFQE. In the thrombolitic therapy group, HFAV provided similar information as HFQE. These three measurements-RMSV, HFQE, and HFAV-provide a comprehensive analysis of the high-frequency SAECG for detecting vessel patency and reocclusion. Relative merits of these measures need to be evaluated on a larger database of patients undergoing thrombolysis and angioplasty for acute myocardial infarction.

Increase in rat aortic endothelial free calcium mediated by metabolically sensitive calcium release from endoplasmic reticulum.

OBJECTIVE: The aim was to examine the relationship between cellular metabolism and intracellular [Ca2+] in vascular endothelial cells, focusing on the timing, mechanism, and reversibility of intracellular [Ca2+] changes resulting from ATP depletion. METHODS: Cultured rat aortic endothelial monolayers were loaded with indo-1 and exposed for 30 min to: (1) glucose-free buffer, (2) 10 mM deoxyglucose or iodoacetic acid (0.1 or 2.5 mM) to inhibit glycolysis, or (3) 2 mM NaCN to inhibit oxidative phosphorylation with or without glucose. In other experiments, the pH sensitive fluorescent indicator SNARF-1 was used to assess the relationship between observed changes in [Ca2+] and pH. RESULTS: While glucose deprivation resulted in a minor increase in [Ca2+], glycolytic inhibition resulted in a larger, slowly developing, sustained increase in [Ca2+]. Endothelial [Ca2+] was not affected by inhibition of oxidative phosphorylation alone, whereas a rapid, sustained, and largely reversible increase (approximately 102 nM) occurred when NaCN exposure was combined with glucose deprivation. The increase in [Ca2+] during glucose-free NaCN exposure was not altered when calcium influx was prevented by removal of extracellular calcium, but was abolished following depletion of an intracellular calcium store by the endoplasmic reticular Ca(2+)-ATPase inhibitor thapsigargin. In SNARF-1 loaded monolayers, inhibition of glycolysis with iodoacetic acid decreased intracellular pH by 0.33(SEM 0.10) units whereas inhibition of oxidative phosphorylation in the absence of glucose increased intracellular pH by 0.17(0.05) units. While these divergent pH changes were noted, [Ca2+] increased in both groups. CONCLUSIONS: A metabolically sensitive endoplasmic reticular calcium store is rapidly and reversibly released in vascular endothelial cells. Endothelial [Ca2+] is shown to be dependent on glycolytic energy production. In the endothelial cell, brief periods of inhibition of oxidative phosphorylation in the absence of glucose rapidly affect intracellular calcium pools rather than leading to calcium influx due to non-specific cellular damage. Effects on intracellular pH alone cannot account for the changes in [Ca2+].

High frequency QRS electrocardiography in the detection of reperfusion following thrombolytic therapy.

The hypothesis that an increase in the amplitude (root-mean-square voltage) of the high frequency (150-250 Hz) components of the QRS complex occurs with successful reperfusion following thrombolytic therapy in acute myocardial infarction (AMI) and fails to occur when thrombolysis fails was tested. Clinical markers for successful or failed reperfusion following thrombolytic therapy for AMI are notoriously insensitive. The amplitude of the high-frequency components of the QRS complex decreases during ischemia and returns to normal with resolution of ischemia, but neither the variability in measurement of these potentials nor their patterns of change during the course of AMI have been described. In 32 control subjects, the average coefficient of variation for the amplitude of the high-frequency QRS complex was 10% or 0.3 uV. Based on these data, for the acute infarction population a significant change in this measurement was therefore defined as a change in amplitude > 20% or 0.6 uV on two consecutive recordings. In 30 patients with AMI treated with a thrombolytic agent, either cardiac catheterization, serial serum myoglobin, or complete resolution of ST-segment elevation were used to define successful or failed reperfusion. High-frequency QRS electrocardiograms were obtained at the start of treatment with a thrombolytic agent and for 3 h thereafter using a signal-averaging technique and digital filtering. Standard 12-lead electrocardiograms were obtained at the same time. In patients who reperfused successfully, the high-frequency QRS amplitude increased significantly (1.2 +/- 0.9 uV above its nadir at 83 +/- 36 min after initiation of thrombolytic therapy) in 23 of 25 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Direct and indirect cost of percutaneous transluminal coronary angioplasty.

A prospective study of 53 patients employed in the 6-month period before coronary angioplasty was performed to determine the direct and indirect costs of lag time in work resumption. The total direct costs calculated were $273,480; indirect costs for this sample were $150,944. When these costs are generalized to all patients in the US undergoing uncomplicated percutaneous transluminal coronary angioplasty, the costs are more than $1.2 billion. This study demonstrated that even in patients with a high a priori probability of work return, delay in work resumption results in a greater cost to the individual and society through absence from the labor force.

Effect of blockade of the ATP-sensitive potassium channel on metabolic coronary vasodilation in the dog.

The hypothesis that the ATP-sensitive potassium channel provides the link between change in coronary blood flow and myocardial oxygen demand was tested in 9 dogs instrumented to measure coronary flow and regional wall thickening in the basal state and at a high level of myocardial oxygen consumption produced by systemic infusion of phenylephrine and simultaneous atrial pacing at an elevated heart rate. Measurements were recorded before and after blockade of ATP-sensitive potassium channels with intracoronary glibenclamide (2 mumol/min). While glibenclamide reduced the absolute level of coronary flow in the basal state, the increase in flow due to increased metabolic demand was unchanged compared with control. Thus, activity of the ATP-sensitive potassium channel determines the set point from which adjustments of coronary flow in response to metabolic stimuli occur, but does not provide a link between changes in oxygen demand and changes in coronary flow.

Ultrasound guided ablation of pseudoaneurysm following coronary artery stent placement: a preliminary report.

A femoral artery pseudoaneurysm in a 47 year old woman following coronary artery stent placement was treated with color-flow duplex ultrasound guided compression. This technique may be useful following stent placement because of the requirement for continued anticoagulation post-procedure.

Blockade of the ATP-sensitive potassium channel modulates reactive hyperemia in the canine coronary circulation.

The mechanism of reactive hyperemia remains unknown. We hypothesized that reactive hyperemia was related to the opening of ATP-sensitive potassium channels during coronary occlusion. The resulting hyperpolarization of the smooth muscle cell plasma membrane might reduce calcium influx through voltage-dependent calcium channels and result in relaxation of smooth muscle tone and vasodilation. In eight open-chest, anesthetized dogs, 30-second coronary occlusions resulted in an average flow debt repayment of 200 +/- 41%. After low-dose (0.8 mumol/min) and high-dose (3.7 mumol/min) infusion of intracoronary glibenclamide, flow debt repayment fell to 76 +/- 14% and 50 +/- 8%, respectively (p less than 0.05 compared with control for both). The decline in flow debt repayment was due to a significant reduction both in maximum coronary conductance during reactive hyperemia and in its duration. In addition, there was a significant decline in the sensitivity of the coronary circulation to adenosine-induced vasodilation after glibenclamide. While more variable, there was no overall change in the sensitivity of the coronary vasculature to acetylcholine-induced vasodilation after glibenclamide. We conclude that reactive hyperemia is determined in a large part by the ATP-sensitive potassium channel, probably through its effect on membrane potential and voltage-sensitive calcium channels. Because reactive hyperemia was never fully abolished at the highest doses of glibenclamide tested, it is possible that additional mechanisms are involved in the genesis of this complex phenomenon.

Effect of perfusate rheology on the diastolic coronary pressure-flow relationship.

The hypothesis that rheological properties of the coronary perfusate account for the curvilinearity and high zero-flow pressure (Pf = 0) of the diastolic coronary-pressure flow relationship (DCPFR) was tested by measuring these relationships using coronary perfusates of varying rheological character. In 16 open-chest, heart-blocked dogs the left circumflex coronary artery was cannulated and perfused using an extra-corporeal circuit, and autoregulation was abolished with intracoronary adenosine. DCPFRs were constructed from data obtained at multiple steady-state levels of coronary pressure during long diastoles while left ventricular diastolic pressure was held constant. Although isovolumic hemodilution reduced hematocrit from 46 +/- 3% to 32 +/- 3% and increased coronary conductance, it neither abolished the curvilinearity nor changed Pf = 0, which remained significantly higher than left ventricular diastolic pressure. In 10 additional animals, DCPFRs obtained during blood perfusion were compared with those obtained using crystalloid perfusate. Crystalloid perfusion increased coronary conductance and failed to abolish curvilinearity. However, with crystalloid perfusate, Pf = 0 was reduced to a value essentially equal to left ventricular diastolic pressure. We conclude that while the rheological properties of coronary perfusates do not fully account for the curvilinearity of the DCPFR, they do importantly influence coronary conductance and Pf = 0.

Coronary artery aneurysm formation following percutaneous transluminal coronary angioplasty: treatment of associated restenosis with repeat percutaneous transluminal coronary angioplasty.

Restenosis following coronary angioplasty can usually be treated effectively and safely by repeated angioplasty. However, the presence of a complex lesion morphology may bias the clinician away from angioplasty toward either recommending bypass surgery or continuing medical therapy alone in spite of recurrence of the symptoms which were sufficient indication for the initial angioplasty. One type of complex morphology at the site of the restenosis is due to the presence of a focal, eccentric aneurysmal dilatation similar in appearance to a saccular aneurysm. In two previously reported cases in the literature both were referred to bypass surgery. We report eight additional cases including the use of repeat successful angioplasty in six of the cases in spite of the potential problems posed by the complexity of the restenosed lesion. In addition, this case review suggests that this type of complex lesion morphology with restenosis may be more common when the initial angioplasty was associated with deep arterial injury, as in patients whose initial angioplasty was done in an infarct-related vessel or was associated with evidence of a large dissection.

Effect of ischemic zone size on nonischemic zone function.

To study the influence of ischemic zone size on function in nonischemic regions, wall thickening and the end-systolic pressure-thickness (ESPTR) relationship were measured before and during a 90-s coronary occlusion, which produced either a small or large (24 or 35% of left ventricular mass) area of ischemia. With both size ischemic areas, nonischemic zone isovolumic and ejection phase wall thickening increased during occlusion, primarily because of increased preload and, to a lesser extent, a reduced pressure component of afterload. The nonischemic region ESPTR was unchanged from preocclusion control with small ischemic mass. With larger ischemic mass, the nonischemic region ESPTR was shifted downward and to the left, indicating reduced end-systolic performance. The decline in the nonischemic zone ESPTR with large ischemic zone size was not due to reduced blood flow, shortening deactivation, reflex effects, or "tethering" but rather to the associated decline in coronary perfusion pressure. Thus the increase of nonischemic region wall thickening during acute ischemia is due to a change in ventricular loading conditions and not augmentation of contractile performance. Larger ischemic zone size can impair function in nonischemic myocardium by reducing the erectile component of end-systolic performance.

Preservation of coronary flow reserve in stunned myocardium.

Microvascular obstruction and persistent focal ischemia have been suggested as a possible cause of myocardial dysfunction (stunning) after brief coronary occlusion. Microvascular occlusion should result in a reduction in maximal coronary flow reserve, although resting transmural coronary flow may be maintained by release of local vasodilators, such as adenosine. To test the microvascular occlusion hypothesis, coronary flow reserve was measured in 14 anesthetized dogs, before and after myocardial stunning produced by 10 min of ischemia. Intracoronary adenosine infusion (5,900 microM/min) increased coronary flow to the same degree in normal [195 +/- 20 (SE) ml/min] and stunned (212 +/- 23 ml/min) myocardium. Peak hyperemic flow after 100 s of coronary occlusion was also similar in normal (205 +/- 25 ml/min) and stunned (218 +/- 23 ml/min) myocardium. The adenosine antagonist 8-phenyltheophylline (5 mg/kg) reduced the flow response to exogenous adenosine, but neither resting coronary flow nor peak hyperemic flow in stunned myocardium was altered. In stunned myocardium, myocardial shortening at rest (0.2 +/- 2.0%) increased during reactive hyperemia (to 13.8 +/- 2.5%, P less than 0.01), but shortening promptly returned to basal levels after each hyperemia. These findings indicate that fixed microvascular occlusion is unlikely to be an important factor in the pathogenesis of stunned myocardium and that local adenosine release does not appear to have a compensatory role in coronary vasoregulation in stunned myocardium.

Double vs single balloon technique for aortic balloon valvuloplasty.

Percutaneous aortic valvuloplasty using a single dilating balloon has been associated with significant but modest reduction in transvalvular pressure gradient and increase in valve area. The balloon diameter is usually 20 mm or smaller to avoid disruption of aortic root structure and to permit forward blood flow during inflation. To evaluate the safety and efficacy of valvuloplasty using a combination of balloons with larger maximum inflated diameters, we compared results of aortic valvuloplasty in 21 patients using either the single or double balloon technique. Mean maximum inflated balloon diameter was 19.4 mm +/- 1.4 for the single balloon technique, while the mean sum of diameters for the simultaneous double balloon technique was 36.3 mm +/- 3.9. The mean age, aortic annulus diameter, and predilatation aortic valve area were not different among groups. Mean aortic transvalvular gradient reduction and mean aortic valve area increase were greater for the double balloon technique. The procedure was well tolerated with no major complications. No change in the degree of aortic regurgitation was noted. The double balloon technique for aortic valvuloplasty is safe and more effective at improving aortic valve area and transvalvular gradient than the conventional single balloon technique.

Effect of afterload resistance on end-systolic pressure-thickness relationship.

The influence of afterload resistance on the end-systolic pressure-thickness relationship (ESPTR) was assessed in six isolated canine left ventricles made to eject into a simulated arterial system. An increase of simulated peripheral resistance from 1.5 to 6.0 mmHg.s.ml-1 resulted in a modest but significant shift of the ESPTR upward and to the right, indicating augmented contractile performance. A relationship between the extent of systolic wall thickening and end-systolic performance was also observed: increased wall thickening impairing and decreased wall thickening enhancing end-systolic performance. The dependence of end-systolic performance on wall thickening history in this setting is consistent with shortening deactivation. This phenomenon appears to account at least in part for the observed shift in the ESPTR with altered afterload resistance.