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Biomedical subjects

J E Parrillo

Publications and source records attributed to J E Parrillo.

At least 55 records · Page 3Linked to original sources
PubMed1999

Role of nitric oxide and cGMP in human septic serum-induced depression of cardiac myocyte contractility.

Previous studies have demonstrated the existence of a circulating myocardial depressant substance during human septic shock. We have recently identified this substance as a synergistic combination of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). This study utilized an in vitro cardiac myocyte assay to evaluate the potential mechanistic role of nitric oxide (NO) and cGMP in depression of myocyte contractility induced by TNF-alpha, IL-1beta, TNF-alpha + IL-1beta (at low concentrations), and human septic shock serum (HSS). TNF-alpha, IL-1beta, TNF-alpha + IL-1beta, and each of 5 sera from patients with acute septic shock caused depression of both maximum extent and peak velocity of cardiac myocyte shortening and an increase in intracellular cGMP concentration during 30 min of exposure (minimum P < 0.01). NO synthetase (NOS) and guanylate cyclase inhibitors such as N-methyl-L-arginine (L-NMA) and methylene blue prevented these effects; an excess of L-arginine with L-NMA restored them (minimum P < 0.01). In contrast, D-arginine failed to reestablish cytokine-induced myocyte depression and cGMP accumulation prevented by L-NMA. Exposure of myocytes to TNF-alpha, IL-1beta, or TNF-alpha + IL-1beta produced a concentration-dependent increase in intracellular cGMP that paralleled the depression of cardiac myocyte contractility (minimum P < 0.001). In addition, TNF-alpha, IL-1beta, TNF-alpha + IL-1beta, or HSS application to cardiac myocytes resulted in increased NO gas generation, which was inhibited by L-NMA (minimum P < 0.01). Furthermore, unstimulated cardiac myocytes were shown to harbor constitutive but not inducible NOS activity. These data suggest that the sequential generation of NO by a constitutive NOS and cGMP by guanylate cyclase represents an important mechanism of cardiac myocyte depression by TNF-alpha, IL-1beta, TNF-alpha + IL-1beta, and the myocardial depressant substance(s) of septic shock.

Animals↗
PubMed1998

Value of the American College of Cardiology/American Heart Association stenosis morphology classification for coronary interventions in the late 1990s.

The goal of this study was to reassess the accuracy of the American College of Cardiology/American Heart Association (ACC/AHA) stenosis morphology classification for predicting coronary intervention success and complications in the era of new devices. Previous studies performed in the early part of this decade for percutaneous transluminal coronary angioplasty in patients with multivessel coronary artery disease found that these criteria were predictive of success rates but not complication rates. Data for 957 consecutive coronary interventions in 1,404 lesions from June 1994 to October 1996 were prospectively classified according to ACC/AHA guidelines and entered into a database. Ninety-one and 9/10 of coronary interventions were successful, defined as <50% residual stenosis of each vessel attempted in the absence of major in-hospital complications, including Q-wave myocardial infarction, ventricular arrhythmia, need for emergency coronary artery bypass surgery, or death. Success rates did not differ between A (186 of 193, 96.3%), B1 (211 of 221, 95.5%), and B2 (676 of 711, 95.1%) lesions, but each was more successful than C (246 of 279, 88.2%) lesions (p <0.003, p < 0.004, and p = 0.0001, respectively). The class of lesion (A, B, or C) did not predict device (atherectomy, rotablator, and stent) use but specific morphologic characteristics of lesions within these classes were predictive of which device was used. Multiple regression analysis revealed that total occlusion and vessel tortuosity were predictive of procedure failure. Lesion type (A, B, or C) was not predictive of complications, but bifurcation lesions (p = 0.0045), presence of thrombus (p = 0.0001), inability to protect a major side branch (p = 0.0468), and degenerated vein graft lesions (p = 0.0283) were predictive. Thus, the ACC/AHA grading system is predictive of successful coronary intervention outcome, particularly of C-type characteristics, but not of complications or device success rate and selection. Although lesion type (A, B, or C) was not predictive of complications, specific lesion morphologies were predictive of adverse events and device use.

Aged↗
PubMed1998

Improved risk stratification in unstable angina: identification of patients at low risk for in-hospital cardiac events by admission echocardiography.

BACKGROUND: Current protocols for risk stratification of patients with acute chest pain syndromes rely on clinical parameters and are oriented toward identification of patients at high risk for adverse cardiac events; however, this paradigm for risk stratification does not adequately address the observation that adverse cardiac events are relatively uncommon in this population. In an era of cost containment, consideration also should be given to identification of patients at low risk for adverse cardiac events, who may be safely discharged without expensive inpatient hospitalization. HYPOTHESIS: The purpose of this study was to develop echocardiographic predictors that identify unstable angina patients at low risk for adverse cardiac events and that discriminate between low- and high-risk patients. METHODS: The predictive accuracy of retrospectively determined echocardiographic predictors were compared in a population-based sample of 66 consecutive unstable angina patients undergoing echocardiography within 24 h of admission. RESULTS: Echocardiographic predictors of adverse events included wall motion score index > or = 0.2, ejection fraction < or = 40%, and mitral regurgitation severity > 2. One or more echocardiographic predictors of adverse events were present in 32 patients (48%). A composite echocardiographic predictor of adverse events was specific, had a high positive predictive value for the identification of high-risk patients, and discriminated between unstable angina patients at high and low risk for adverse cardiac events. CONCLUSION: Echocardiographic predictors of adverse events are specific and discriminate between unstable angina patients at high and low risk for adverse cardiac events.

Acute Disease↗
PubMed1998

Metabolic fate of glucose in vascular smooth muscle during contraction induced by norepinephrine.

The metabolism of glucose in porcine carotid artery was tracked by isotopic methods during sustained isometric contraction induced by 100 microM norepinephrine (NE). In resting muscles, 74 and 18% of glucose taken up was accounted for by glycolysis and glycogen synthesis, respectively. Lactate production accounted for 69%, pyruvate production for 12%, and glucose oxidation accounted for 14% of glycolytic flux. The oxidation of glucose accounted for 57% of the consumption of O2 and thus constituted the primary oxidative substrate. During contraction by NE, glucose-uptake declined modestly below the resting basal rate. Glycolysis of external glucose and lactate production decreased and then increased with sustained contraction. Norepinephrine stimulated simultaneous glycogenolysis and glycogen synthesis, with net glycogen synthesis prevailing over 90 min of isometric contraction. Furthermore, NE modified the distribution of glucosyl units throughout the glycogen pool. The steady state rate of oxidation of glucose did not increase during NE contraction, even though O2-consumption increased. In contrast, increased glucose oxidation was demonstrable during contraction induced by 80 mm KCl. Furthermore, oxidation of exogenous fatty acid could be demonstrated during NE-induced contraction. Thus, NE exerts multiple effects on glucose and glycogen metabolism in smooth muscle, but it does not stimulate glucose oxidation.

Animals↗
PubMed1998

Malate-aspartate shuttle, cytoplasmic NADH redox potential, and energetics in vascular smooth muscle.

The effect of inhibition of the malate-aspartate shuttle on the cytoplasmic NADH/NAD ratio and NADH redox state and its corresponding effects on mitochondrial energetics in vascular smooth muscle were examined. Incubation of porcine carotid arteries with 0. 4 mmol amino-oxyacetic acid an inhibitor of glutamate-oxaloacetate transaminase and, hence the malate-aspartate shuttle, inhibited O2 consumption by 21%, decreased the content of phosphocreatine and inhibited activity of the tricarboxylic acid cycle. The rate of glycolysis and lactate production was increased but glucose oxidation was inhibited. These effects of amino-oxyacetic acid were accompanied by evidence of inhibition of the malate-aspartate shuttle and elevation in the cytoplasmic redox potential and NADH/NAD ratio as indicated by elevation of the concentration ratios of the lactate/pyruvate and glycerol-3-phosphate/dihydroxyacetone phosphate metabolite redox couples. Addition of the fatty acid octanoate normalized the adverse energetic effects of malate-aspartate shuttle inhibition. It is concluded that the malate-aspartate shuttle is a primary mode of clearance of NADH reducing equivalents from the cytoplasm in vascular smooth muscle. Glucose oxidation and lactate production are influenced by the activity of the shuttle. The results support the hypothesis that an increased cytoplasmic NADH redox potential impairs mitochondrial energy metabolism.

Aminooxyacetic Acid↗
PubMed1998

Clinical predictors easily obtained at presentation predict resource utilization in unstable angina.

OBJECTIVE: To determine if a risk prediction model for patients with unstable angina would predict resource utilization. METHODS AND RESULTS: Four hundred sixty-five consecutive patients admitted for unstable angina to a tertiary care university-based medical center were prospectively evaluated from June 1, 1992, to June 30, 1995. The proportion of patients receiving coronary angiography, coronary angioplasty, and coronary artery bypass grafting were analyzed according to four risk groups on the basis of a previously published model: Group 1, <2% risk of major complication; Group 2, 2.1% to 5% risk; Group 3, 5.1 % to 15% risk; and Group 4, >15.1 % risk. Hospital length of stay and estimated cost of hospitalization based on DRG and specific payer ratio of cost-to-charge were also compared between groups. Multiple linear regression analysis was used to determine the influence of estimated risk and procedures on hospital costs. The four groups were well matched for gender, hypertension, tobacco history, and previous percutaneous transluminal coronary angioplasty and myocardial infarction. Group 4 had a higher incidence of previous coronary bypass grafting (35% vs 10%, p=0.001) and triple vessel or left main coronary artery disease compared with Group 1 (44% vs 13%, p=0.041). Group 4 patients were more likely to be admitted to the coronary care unit compared with Group 2 or Group 1 patients (80% vs Group 1: 51% [p= 0.001]; and vs Group 2: 53% [p=0.001]), more likely to receive heparin (87% vs 71%, p=0.007), and more likely to receive a beta-blocker or calcium channel blocker (89% vs 74%, p=0.008) than Group 1. Coronary angioplasty rates were similar for all groups, but Group 4 patients were more likely to receive coronary bypass grafting than Group 2 or Group 1 (27% vs Group 2: 12%, p=0.004 and vs Group 1: 8%, p=0.002). Hospital length of stay was highest in Group 4 and lowest for Group 1. Average hospital costs were significantly less in Group 3 than in Group 4, but higher than in Group 1. Multivariate analysis determined a dependency of costs on risk group with Group 2 having costs 31.4% (95% CI=9.8 to 57.2), Group 3 46.7% (24, 3 to 73.1), and Group 4 75% (46.9 to 110.7) higher than Group 1. The use of procedures also significantly increased costs, with PTCA-treated patients having a 44.9% (26.7 to 65.7) increase in costs compared with medically treated patients, and surgically treated patients having a 204.7% increase in costs. CONCLUSION: Resource utilization as assessed by the use of revascularization procedures, length of stay, and hospital costs are influenced by patient acuity estimated from a prediction model on the basis of estimated risk of cardiac complications. The model exerts independent influence on cost even after adjustment for various procedures. The use of revascularization procedures, especially coronary artery surgery, remains a large determinant of hospital cost.

Adult↗
PubMed1998

Accurate noninvasive estimation of left ventricular end-diastolic pressure: comparison with catheterization.

We evaluated the accuracy of a new Doppler-based method using the mitral regurgitant velocity at the time of aortic valve opening for the noninvasive estimation of left ventricular end-diastolic pressure. Sixty unselected patients were studied immediately before routine catheterization. Invasive left ventricular end-diastolic pressure was obtained using a fluid-filled pig-tail catheter. Noninvasive estimation of left ventricular pressure at aortic valve opening was taken as systemic diastolic pressure using an automated cuff. Noninvasive left ventricular end-diastolic pressure was calculated as diastolic blood pressure--4 x (mitral regurgitant velocity at aortic opening)2. Those making noninvasive determinations were blinded to catheterization results. An adequate mitral regurgitant Doppler recording was obtained in 24 patients (40%). In patients with a left ventricular end-diastolic pressure greater than 15 mm Hg the yield was 65%. Left ventricular end-diastolic pressures ranged from 4 mm Hg to 30 mm Hg. Bland and Altman analysis revealed no systematic bias and close agreement was found, with individual discrepancies not exceeding 5 mm Hg.

Blood Pressure↗
PubMed1998

Randomized, blinded, placebo-controlled trial of tissue factor pathway inhibitor in porcine septic shock.

This study tested the hypothesis that tissue factor pathway inhibitor (TFPI) would improve mortality and morbidity evoked by peritonitis-induced bacteremia in pigs. Secondarily, it sought to determine if TFPI treatment would attenuate cardiodynamic abnormalities produced by this septic model. 32 pigs were chronically instrumented with intracardiac transducers to measure left ventricular pressure and diameter, pulmonary and aortic pressures, and cardiac output. At least 5 days after surgery to implant transducers, basal cardiovascular readings and blood samples were obtained. Using a randomized, blinded study design, either purified, reconstituted TFPI (1 mg/kg bolus, 10 mg/kg/min for 48 h), placebo (arginine buffer), or saline was administered to pigs immediately after Escherichia coli 0111.B4 (3.0-11 x 10(9) colony-forming U/kg)-laden fibrin clots were implanted intraperitoneally, producing peritonitis and bacteremia. Pigs did not receive antibiotics or supportive therapy. No significant differences in primary or secondary endpoints were noted between the arginine and saline groups, so these data were combined into a control group (N = 20). 5 of 12 TFPI pigs survived (42%), while 5 of 20 control pigs survived (25%); this difference was not significant (p = .714, Fisher's exact test). TFPI treatment augmented cardiac output in surviving pigs, but did not affect any other cardiovascular performance variable (heart rate, % diameter shortening, or systemic and pulmonary vascular resistance). In controls, peritonitis induced rapid increase in plasma tumor necrosis factor-alpha (428 +/- 771 to 5,933 +/- 559 pg/mL at 2 h) and interleukin-8 (180 +/- 153 to 1,393 +/- 145 pg/mL at 2 h). TFPI treatment significantly attenuated cytokine responses to sepsis, reducing peak tumor necrosis factor-alpha to 2,103 +/- 813 pg/mL and reducing peak interleukin-8 levels to 534 +/- 211 pg/mL at 2 h (p < .05, Tukey test, two-way ANOVA). In conclusion, TFPI treatment attenuated important mediator components of the inflammatory response but did not provide significant survival benefit.

Animals↗
PubMed1998

Discordant epicardial and microvascular endothelial responses in heart transplant recipients early after transplantation.

BACKGROUND: Cardiac allograft vasculopathy represents the leading cause of death in heart transplant recipients who survive more than 1 year. Functional endothelial abnormalities are sensitive measures of the early development of cardiac allograft vasculopathy, but the relative importance of large and small coronary vessel abnormalities has not been evaluated. The purpose of the study was to distinguish between large and small coronary endothelial dysfunction in patients early after heart transplantation and to test the hypothesis that microvascular endothelial responses can be preserved in the presence of epicardial endothelial dysfunction. METHODS: Changes in epicardial lumen area and coronary artery blood flow in response to intracoronary administration of adenosine, acetylcholine, and nitroglycerin were measured simultaneously by use of an intravascular ultrasound catheter positioned over a Doppler flow wire in the left anterior descending coronary artery. The combination of these techniques allowed distinction between large and small coronary vascular responses. In 19 patients studied early after transplantation, adenosine (16 and 32 microg), acetylcholine (5.4 and 54 microg), and nitroglycerin (200 microg) were infused, with continuous intravascular ultrasound imaging and Doppler velocity measurements. RESULTS: Acetylcholine induced paradoxical epicardial vasoconstriction in 12 of 19 patients (73% +/- 6% of baseline); vasodilation occurred in 7 (108% +/- 3%). In spite of this constriction, coronary artery flow increased in all 19 patients, to the same extent in patients with constriction and those with dilation (239 +/- 26 vs 193 +/- 20, p = 0.38). Adenosine and nitroglycerin increased area (107% +/- 1% and 112% +/- 3%) and flow (258% +/- 17% and 197% +/- 11%) in all patients. None of the area or flow responses correlated with the degree of intimal thickening. CONCLUSIONS: Acetylcholine increased coronary artery flow early after transplantation, indicating preserved microvascular responses in spite of epicardial vasoconstriction. Simultaneous measurement of area and velocity responses, by permitting evaluation of the relative contribution of epicardial and microvascular vessels, may offer unique insights into coronary endothelial function.

Acetylcholine↗
PubMed1998

The use of APACHE II scores to select candidates for left ventricular assist device placement. Acute Physiology and Chronic Health Evaluation.

BACKGROUND: The growth in left ventricular assist device (LVAD) use has been hampered by high morbidity and mortality rates and cost. The purpose of this study was to help improve patient selection for LVAD placement by determining whether the Acute Physiology and Chronic Health Evaluation II (APACHE II) scoring system, a multiparameter, physiology-based predictor of outcome, could be used to predict outcome after LVAD placement and thus help determine optimum timing of LVAD placement. METHODS: This was a retrospective analysis of a prospective cohort observational study consisting of 2 groups: (1) 50 patients with severe heart failure who did not receive LVAD placement after initial evaluation and (2) 31 patients who did receive LVAD placement. Patients included in the study were in severe heart failure on the basis of 3 of the following: lung crackles, S3, peripheral edema, ejection fraction < 0.30, systolic blood pressure < 80 mm Hg, progressive prerenal azotemia, altered level of consciousness, gastrointestinal ischemia or congestion, or persistent although reversible pulmonary hypertension in spite of maximal medical therapy, including intravenous inotropes. The decision for LVAD placement was at the discretion of the attending physician. RESULTS: Both LVAD- and non-LVAD-treated patients were similar in cause of heart failure, APACHE II scores, and other baseline laboratory parameters. Survival time with a log-logistic model was better for LVAD-treated patients, p=.0266. Although Kaplan Meier analysis showed a trend toward better survival rates in the LVAD-treated patient, the Cox proportional hazards revealed that LVAD-treated patients had better survival (relative risk ratio, 95% confidence interval=0.305, 0.110 to 0.892; p=.0219) after adjustment for APACHE II score. Each unit increase in APACHE II independently predicted death (relative risk ratios, 95% confidence interval=1.139, 1.055 to 1.231; p=.0009). Patients with medium APACHE II (11 to 20) scores in particular benefitted from LVAD treatment. CONCLUSION: LVAD placement for severe heart failure (not restricted to cardiogenic shock) improves survival. APACHE II can aid in deciding the timing of LVAD placement in patients with heart failure who may not have attained conventional hemodynamic criteria for LVAD placement. Patients who had APACHE II scores between 11 and 20 derived the greatest benefit from LVAD placement.

APACHE↗
PubMed1997

Oxidation of acetate and octanoate and its relation to glucose metabolism in contracting porcine carotid artery.

The oxidation of octanoate and acetate was measured in segments of porcine carotid arteries to ascertain whether the oxidation of exogenous fatty acid substrates (acetate and octanoate) is augmented during contraction induced by K(+)-depolarization. The oxidation of acetate increased from 7 +/- 1 to 14 +/- 2 nmol/min/g (P < 0.01) during sustained isometric contraction. Octanoate oxidation increased from 11 +/- 1 to 14 +/- 1 nmol/min/g (P < 0.05). The rate of oxidation of neither acetate nor octanoate was affected by the presence or absence of glucose either in resting or contracting arteries Acetate or octanoate oxidation could account for the majority of O2 consumption during contraction. Octanoate but not acetate inhibited glucose uptake and glycolysis in resting muscles. In contrast to augmented acetate and octanoate metabolism during contraction, there was a "down-regulation" of glucose metabolism in contracting muscles as evidenced by a decrease in the rate of glucose uptake, glycolysis and lactic acid production during sustained isometric contraction. Thus, contractile activation of vascular smooth muscle is associated with a shifting pattern of substrate utilization. Exogenous acetate or octanoate can serve as the primary oxidative substrate during sustained isometric contraction.

Acetates↗
PubMed1997

Comparison of heparin therapy for < or = 48 hours to > 48 hours in unstable angina pectoris.

Of 450 consecutive patients with unstable angina admitted to a tertiary care, university-based medical center over a 24-month period, 334 were administered heparin and aspirin for some length of time. Two groups of 98 patients matched for acuity and gender at baseline were treated with either < or = 48 hours (group 1) or > 48 hours (group 2) of heparin. The acuity model used in this study incorporates 6 factors: age, recent myocardial infarction, treatment with intravenous nitroglycerin, previous therapy with beta blockers or calcium antagonists, baseline ST depression, and diabetes. Despite similar risks and overall clinical outcome, group 2 had significantly more myocardial infarction or death after 48 hours than group 1 (p = 0.01). In part, this was due to a delay in the performance of coronary angiography (2.8 +/- 1.4 vs 3.5 +/- 15 days, p = 0.01), coronary intervention (2.7 +/- 1.8 vs 5.1 +/- 2.3 days, p = 0.01), and bypass surgery (3.8 +/- 3.6 vs 7.0 +/- 5.6 days, p = 0.02). There was no difference between groups regarding the success of coronary intervention (90% vs 88%, p = NS). Heparin duration was influenced by the finding of intracoronary thrombus or ulceration on angiography before revascularization, as each finding was seen more often in group 2 (thrombus, 12% vs 24%; ulceration, 38% vs 60%). These results suggest that the optimal duration of heparin therapy is up to 48 hours after admission in unstable angina; a longer time period is associated with increased adverse consequences.

Aged↗
PubMed1997

Cytoplasmic redox potential affects energetics and contractile reactivity of vascular smooth muscle.

Variations in the cytoplasmic redox potential (Eh) and NADH/NAD ratio as determined by the ratio of reduced to oxidized intracellular metabolite redox couples may affect mitochondrial energetics and alter the excitability and contractile reactivity of vascular smooth muscle. To test these hypotheses, the cytoplasmic redox state was experimentally manipulated by incubating porcine carotid artery strips in various substrates. The redox potentials of the metabolite couples [lactate]/[pyruvate]i and [glycerol 3-phosphate]/[dihydroxyacetone phosphate]i varied linearly (r=0.945), indicating equilibrium between the two cytoplasmic redox systems and with cytoplasmic NADH/NAD. Incubation in physiological salt solution (PSS) containing 10 mm pyruvate ([lact]/[pyr]=0.6) increased O2 consumption approximately 45% and produced anaplerosis of the tricarboxylic acid (TCA cycle), whereas incubation with 10 mm lactate-PSS ([lact]/[pyr]i=47) was without effect. A hyperpolarizing dose of external KCl (10 mM) produced a decrease in resting tone of muscles incubated in either glucose-PSS (-0.8+/-0.8 g) or pyruvate-PSS (-2.1+/-0.8 g), but increased contraction in lactate-PSS (1.5+/-0.7 g) (n=12-18, P<0.05). The rate and magnitude of contraction with 80 mm KCl (depolarizing) was decreased in lactate-PSS (P=0.001). Slopes of KCl concentration-response curves indicated pyruvate>glucose>lactate (P<0.0001); EC50 in lactate (29. 1+/-1.0 mM) was less than that in either glucose (32.1+/-0.9 mm) or pyruvate (32.2+/-1.0 mM), P<0.03. The results are consistent with an effect of the cytoplasmic redox potential to influence the excitability of the smooth muscle and to affect mitochondrial energetics.

Aerobiosis↗
PubMed1997

Does low individual operator coronary interventional procedural volume correlate with worse institutional procedural outcome?

OBJECTIVES: To assess the relation between individual operator coronary interventional volume and incidence of complications, the in-hospital outcome at a single, moderate volume urban academic center was prospectively collected over a 3-year period. BACKGROUND: A minimum of 75 coronary interventions/operator per year may be required in the future to obtain formal certification. However, few data exist regarding individual operator volumes and procedural outcome. METHODS: Between January 1993 and December 1995, 1,389 consecutive procedures were performed or supervised by nine geographic full-time operators: 171 (12.3%) utilized various devices, and 350 (25.2%) involved multivessel coronary intervention. Left ventricular ejection fraction was 59 +/- 15% (mean +/- SD), and there were 1.7 +/- 0.7 vessels diseased (with > or = 70% stenosis). Clinical indications included stable angina in 22.5% of cases, unstable angina in 31.9%, acute myocardial infarction (MI) in 2.9%, post MI in 20.6%, shock or acute heart failure in 3.0% and restenosis in 19.1%. In the last consecutive 857 lesions in 655 cases, 20.7% type A, 55.5% type B and 23.8% type C lesions were categorized before coronary intervention. RESULTS: Average yearly operator volume ranged from 26 to 83 cases (mean 51 +/- 26). Each operator has performed a total of 590 +/- 268 coronary interventions, with 10.0 +/- 4.3 years of coronary interventional experience. The mean angioplasty volume rating for the nine operators was 180 +/- 37 (> 170 considered adequate). The in-hospital major complication rate was 1.4% (95% confidence interval 0.7% to 1.893%) for all coronary interventions, including death in 3 patients, bypass surgery in 13, arrhythmia in 3 and Q wave MI in 2. To ascertain how these outcomes compared with standard measures of coronary interventional outcome, four previously published registries were reanalyzed in a similar manner. The rate of complications in the present study was found to be significantly lower than that of the 1992-1993 Society for Cardiac Angiography and Intervention registry (1.9%, n = 19,594, p < 0.05 [excludes ventricular arrhythmias]), the 1994 American College of Cardiology database (3.9%, n = 38,963, p = 0.001), the Mid-America Heart Institute outcome in 1988 (2.3%, n = 5,413, p = 0.02) and the 1985-1986 National Heart, Lung, and Blood Institute Registry (7.2%, n = 1,801, p = 0.001). Odds ratios and 95% confidence intervals showed the outcome in the current study to be at least comparable to the standard registries. CONCLUSIONS: Despite individual operator volumes below those currently being considered for credentialing, the overall institutional outcome was excellent in a diverse and complex patient population.

Academic Medical Centers↗
PubMed1997

Echocardiography for hemodynamic assessment of patients with advanced heart failure and potential heart transplant recipients.

OBJECTIVES: This study sought to assess the accuracy of Doppler echocardiographic techniques for the determination of right heart catheterization hemodynamic variables in patients with advanced heart failure and in potential heart transplant recipients. BACKGROUND: Doppler echocardiographic techniques permit the noninvasive acquisition of hemodynamic variables traditionally used for the assessment of patients with advanced heart failure and potential heart transplant candidates. However, the accuracy of these techniques has not been sufficiently well documented for clinical application in individual patients. METHODS: Echocardiographic data required for estimation of mean right atrial, pulmonary artery and mean left atrial pressures and cardiac output were obtained. Right heart catheterization was performed immediately after Doppler echocardiographic data were acquired, before any intervention that might have altered the subject's hemodynamic status. RESULTS: A complete Doppler echocardiographic hemodynamic data set was acquired in 21 (84%) of 25 subjects. For all variables, invasive and noninvasive hemodynamic values were highly correlated (p < 0.001), with minimal bias and narrow 95% confidence limits. An algorithm constructed from the noninvasive hemodynamic variable values identified all patients with adverse pulmonary vascular hemodynamic variables (i.e., transpulmonary gradient > or = 12 mm Hg, pulmonary vascular resistance > or = 3 Wood units or pulmonary vascular resistance index > or = 6 Wood units x m2). This algorithm identified 12 (71%) of 19 patients for whom right heart catheterization was unnecessary. CONCLUSIONS: Doppler echocardiographic estimates of hemodynamic variables in patients with advanced heart failure are accurate and reproducible. This noninvasive methodology may assist with monitoring and optimization of medical therapy in patients with advanced heart failure and may obviate the need for routine right heart catheterization in potential heart transplant candidates.

Algorithms↗
PubMed1997

Critical care in the United States. Who are we and how did we get here?

Critical care medicine has progressed significantly over the past two to three decades. We will review the history and evolution of critical care medicine and ICUs in the United States. The evolving health care delivery system and the changing and important role of the intensivist will be addressed. Finally, a discussion about what critical care physicians must do to prepare for the future is presented.

Critical Care↗
PubMed1997

Impaired microvascular vasoconstrictive responses to vasopressin in septic rats.

OBJECTIVE: To evaluate mechanisms of vasodilation in sepsis by comparing responses of resistance arterioles to vasopressin in rat cremaster muscle of septic and control rats. DESIGN: Prospective, experimental study. SETTING: Experimental animal laboratory. SUBJECTS: Twenty male rats, anesthetized with ketamine and acepromazine. INTERVENTIONS: Topical superfusion of vasoactive compounds on skeletal muscle resistance arterioles. MEASUREMENTS AND MAIN RESULTS: The effect of sepsis on responses to local application of vasopressin was investigated using in vivo videomicroscopy. Vasopressin was superfused topically on the cremaster muscle resistance arterioles (15 to 25 microns) of rats made septic by cecal ligation and puncture, and the responses were compared with the responses of controls that underwent sham ligation. Responses to topically suffused vasopressin were also assessed in septic and control rats, before and after superfusion of the muscle with the nitric oxide synthase inhibitor NG-methyl-L-arginine (NMA). Sepsis produced a decrease in the vasoconstrictive effects of vasopressin; the maximal response was lower, and the concentration-response curve was shifted to the right in septic rats (p < .05). Contractions at vasopressin concentrations of 0.01, 1, and 10 nM were 39%, 36%, and 40%, respectively, of sham controls. Superfusion of the muscle with NMA partially restored arteriolar responsiveness in the septic rats, significantly increasing the arteriolar constriction of the septic rats in response to vasopressin. This effect was reversed with superfusion of excess L-arginine (1 mM). CONCLUSIONS: This study illustrates the reduced responsiveness of the resistance arterioles of septic rats in response to vasopressin in vivo, and the partial restoration of responsiveness by concurrent application of NMA. In previous studies using this model, we have shown similar results using norepinephrine and endothelin-1, as well as angiotensin II. These findings, and the findings of this study, suggest a generalized abnormality in responsiveness of resistance arterioles to endogenous vasoconstrictors in sepsis. Partial reversal of this abnormality with NMA supports an important role for nitric oxide in mediating abnormal vasopressor responsiveness in sepsis.

Animals↗