Citations

To improve the predictive accuracy of the signal-averaged electrocardiogram, we created a linear logistic model for predicting ventricular tachycardia during electrophysiologic testing. This signal-averaged electrocardiographic model was created from data obtained from 214 patients undergoing electrophysiologic testing (70 had ventricular tachycardia during electrophysiologic testing) by using stepwise logistic regression to rank eight clinical and nine signal-averaged electrocardiographic variables. The best predictors were ejection fraction, history of infarction, ventricular ectopic pairs or nonsustained ventricular tachycardia on Holter monitoring, QRS duration after 25-Hz filtering, and root mean square voltage of the terminal 40 msec of the QRS complex after 40- and 80-Hz filtering. Cross validation (a statistical technique that can be used to accurately evaluate how a predictive model will perform on a prospective patient population) was used to validate the model. After cross validation, the model's sensitivity was 91% and specificity was 59% for predicting ventricular tachycardia during electrophysiologic testing. This model compared favorably with established 25-Hz late-potential criteria (QRS duration of more than 110 msec and root mean square voltage of less than 25 microV of the terminal 40 msec of the QRS complex; sensitivity, 64%; specificity, 85%) and with established 40-Hz late-potential criteria (QRS duration of more than 114 msec or root mean square voltage of less than 20 microV of the terminal 40 msec of the QRS complex or duration of the low-amplitude signal less than 40 microV at the terminal QRS complex that is greater than 38 msec; sensitivity, 84%; specificity, 54%).(ABSTRACT TRUNCATED AT 250 WORDS)

Studies correlating prosthetic valve gradients determined by continuous wave Doppler echocardiography with gradients obtained by cardiac catheterization have, to date, been limited to patients with mitral and tricuspid prostheses or have compared nonsimultaneous measurements. Simultaneous Doppler and catheter pressure gradients in 36 patients (mean age, 63 +/- 13 years) with 42 prosthetic valves (20 aortic, 20 mitral, one tricuspid, and one pulmonary) were studied. Catheter gradients were obtained using a dual-catheter technique. The simultaneous pressure tracings and Doppler flow velocity profiles were digitized at 10-msec intervals to derive the corresponding maximal and mean gradients. The correlation between the maximal Doppler gradient and the simultaneously measured maximal catheter gradient was 0.94 (SEE = 6), and that between the Doppler gradient and the simultaneously measured mean catheter gradient was 0.96 (SEE = 3). There were no significant differences in correlation between gradients for the 32 mechanical valves (maximal gradients: r = 0.95, SEE = 6; mean gradients: r = 0.96, SEE = 3) and the 10 bioprosthetic valves (maximal gradients: r = 0.89, SEE = 6; mean gradients: r = 0.93, SEE = 3). In patients with mitral prostheses, Doppler gradients correlated well with the corresponding catheter gradients obtained with direct measurement of left atrial pressure (maximal gradients: r = 0.96, SEE = 2; mean gradients: r = 0.97, SEE = 1.2). A close correlation between corresponding Doppler and catheter gradients also was found in patients with aortic prostheses (maximal gradients: r = 0.94, SEE = 6; mean gradients: r = 0.94, SEE = 3). Thus, continuous wave Doppler echocardiography can accurately predict the pressure gradient across prosthetic valves.

The effect of recombinant hirudin and the dosage of heparin on acute platelet-thrombus deposition during carotid angioplasty in anesthetized pigs was prospectively assessed. Fifty-five animals (mean weight, 33.9 kg) were randomized to one of six heparin dosages: heparin boluses of 35, 50, 100, 150, 200, or 250 units/kg followed by a continuous infusion of 35, 50, 100, 150, 200, or 250 units/kg/hr, respectively. Another five pigs received a bolus of 1 mg/kg hirudin (recombinant desulphatohirudin), a specific thrombin inhibitor, followed by an infusion of 1 mg/kg/hr. Bilateral carotid angioplasty was performed in all pigs 20 minutes after starting the infusion; they were sacrificed 57 +/- 12 minutes after the procedure. Deep medial arterial injury was present in approximately 75% of the dilated segments, and subendothelial injury in the remaining 25%. Mean log of number of platelets and molecules of fibrinogen per centimeter squared of deep injury in segments from all the animals treated with heparin were 4.74 +/- 1.03 and 5.02 +/- 0.64, respectively. A regression analysis showed an inverse correlation of the log of platelet deposition with the heparin group (r = -0.56, p = 0.0001) with administered total units of heparin (r = -0.55, p = 0.0003) and with mean plasma heparin concentration (r = -0.55, p = 0.0004) in deeply injured arteries. Similar inverse relations were obtained for fibrinogen. In contrast, the deposition of platelets and fibrinogen in subendothelial injury was very low and independent of the heparin administered.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute occlusion after a successful angioplasty is a severe complication that has been reported in 2-12% of patients. Therefore, to determine whether there was a relation between the dosage of heparin and the presence of mural thrombosis, we studied in a pig model the relation between the dosage of heparin and acute platelet-thrombus deposition on the site of arterial injury. We retrospectively analyzed the effect of three heparin regimens on platelet deposition in 32 normal pigs (mean weight, 32.7 kg) that underwent bilateral carotid angioplasty and were sacrificed 90 +/- 26 minutes later. Pigs in protocol 1 (n = 7) received an intravenous bolus injection of 4,000 units heparin 10 minutes before angioplasty. Pigs in protocol 2 (n = 11) received two bolus injections of 4,000 units heparin 40 minutes apart; the angioplasty was performed immediately after the second bolus. Pigs in protocol 3 (n = 14) had an initial 4,000-unit bolus injection of heparin followed immediately by an infusion of 4,000 units/hr; angioplasty was performed 20 minutes after starting the infusion. 111In-labeled platelet deposition on deeply injured (torn into the media) arterial segments were 86.3 +/- 68, 56.2 +/- 56.9, and 37.7 +/- 37.7 X 10(6)/cm2 for protocols 1, 2, and 3, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract The aim of this study was to examine the role of HDL subparticles with apolipoprotein (apo) A-I alone (LpA-I) and with apoA-I and apoA-II (LpA-I/A-II) in predicting coronary artery disease. Concentrations of these HDL subparticles were compared in 184 subjects with angiographically confirmed significant coronary artery disease (>50% stenosis of at least one vessel) and 191 age- and sex-matched control subjects without clinical coronary artery disease. LpA-I and LpA-I/A-II were measured with magnetic beads coated with anti–apoA-II antibodies to separate particles containing apoA-II from plasma. Total plasma cholesterol and triglyceride levels were similar in both groups. Although subjects with coronary artery disease had lower HDL cholesterol, plasma apoA-I, LpA-I, and LpA-I/A-II than age- and sex-matched control subjects without coronary artery disease, plasma apoA-I was the best predictor of coronary artery disease. In conclusion, LpA-I and LpA-I/A-II are lower in subjects with coronary artery disease but do not add to plasma apoA-I in predicting the presence of coronary artery disease.

Neointimal hyperplasia occurs in the coronary arteries after percutaneous revascularization procedures and is a reparative response that frequently causes recurrent stenosis. Prior animal studies have shown that neointimal tissue thickness is proportional to the depth of arterial injury. Because animal models are increasingly used to test therapeutic strategies against restenosis, the purpose of this study was to evaluate the degree of neointimal thickening formed in the coronary arteries of pigs compared with dogs in response to severe injury. Fourteen coronary arteries in six mongrel dogs and 18 coronary arteries in nine pigs underwent severe arterial injury using tantalum metal coils delivered on oversized angioplasty balloons. Animals were killed after 4 weeks, and all coronary arteries were pressure perfusion fixed. Mean histological injury scores and neointimal thicknesses for dogs were 1.9 +/- 0.3 and 0.30 +/- 0.11, respectively, compared with 2.1 +/- 0.7 and 0.71 +/- 0.36 for pigs. Thus, there was significantly less neointimal thickening in dogs compared with pigs (P < .001) despite no differences in injury (P = NS). The neointimal thickening differences translated into significantly different percent area stenoses: 55 +/- 24% for pigs versus 27 +/- 13% for dogs (P < .001). Linear regression modeled neointimal thickness versus injury assessed by an ordinal injury score proportional to the depth of injury for each species. This analysis confirmed the differences across multiple injury levels. The slope of the regression line for dogs was small, suggesting that no relation may exist between injury and neointimal thickness in this species. The pig may be a more appropriate model for the study of the genesis of stenosing neointima.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract Aims Traditionally, VO2peak has been used to determine prognosis in heart failure; however, this measure has limitations. Hence, other exercise and gas exchange parameters measured submaximally, e.g. breathing efficiency (VE/VCO2), end-tidal CO2 (PETCO2), oxygen uptake efficiency slope (OUES), and circulatory power [ systolic blood pressure (SBP)], have been investigated. The aim of this study was to investigate the prognostic relevance of submaximal exercise gas exchange in heart failure patients. Method and results One hundred and thirty-two consecutive heart failure patients (mean age 56 ± 12 years, ejection fraction 29 ± 11%) performed peak treadmill testing. Gas exchange and haemodynamic variables were measured continuously. Gas exchange data obtained from the first 2 min of exercise and at a respiratory exchange ratio (RER) of 0.9 were the measurements of interest. Over a median follow-up period of 62.4 (range 0–114) months, there were 44 endpoints (death or transplant). Univariate analysis demonstrated submaximal predictors of survival, which included VE/VCO2 slope and ratio, PETCO2, OUES, and circulatory power (P≤ 0.01). When these and additional submaximal variables were included together in the multivariable analysis, the strongest submaximal exercise predictive model (C-statistic 0.75) comprised data from the first stage of exercise (VE and circulatory power) and at an RER of 0.9 (VE/VCO2 ratio). The inclusion of VO2peak and demographic data, with submaximal data (VE/VCO2 ratio at an RER = 0.9), increased the predictiveness of the model (C-statistic 0.78). Conclusion Submaximal exercise measures provide useful prognostic information for predicting survival in heart failure. This form of testing is logistically easier, cheaper, and safer for patients compared with maximal exercise.

The role of venous stasis syndrome (VSS) mechanisms (i.e. venous outflow obstruction [VOO] and venous valvular incompetence [VVI]) on quality of life (QoL) and activities of daily living (ADL) is unknown. The objective of this study was to test the hypotheses that venous thromboembolism (VTE),VSS,VOO and VVI are associated with reduced QoL and ADL. This study is a follow-up of an incident VTE case-control study nested within a population-based inception cohort of residents from Olmsted County, MN, USA, between 1966 and 1990. The study comprised 232 Olmsted County residents with a first lifetime VTE and 133 residents without VTE. Methods included a questionnaire and physical examination for VSS; vascular laboratory testing for VOO and VVI; assessment of QoL by SF36 and of ADL by pertinent sections from the Older Americans Resources and Services (OARS) and Arthritis Impact Measurement Scales (AIMS2) questionnaires. Of the 365 study participants, 232 (64%), 161 (44%), 43 (12%) and 136 (37%) had VTE, VSS, VOO and VVI, respectively. Prior VTE was associated with reduced ADL and increased pain, VSS with reduced physical QoL and increased pain, and VOO with reduced physical QoL and ADL.VVI was not associated with QoL or ADL. In conclusion,VSS and VOO are associated with worse physical QoL and increased pain. VOO and VTE are associated with impaired ADL. We hypothesize that rapid clearance of venous outflow obstruction in individuals with acute VTE will improve their QoL and ADL.

Background— Reductions in numbers of circulating progenitor cells (CD34+ cell subsets) have been demonstrated in patients at risk for, or in the presence of, cardiovascular disease. The mediators of these reductions remain undefined. To determine whether neurohumoral factors might regulate circulating CD34+ cell subsets in vivo, we studied complementary canine models of left ventricular (LV) dysfunction. Methods and Results— A pacing model of severe LV dysfunction and a hypertensive renal wrap model in which dogs were randomized to receive deoxycorticosterone acetate (DOCA) were studied. Circulating CD34+ cell subsets including hematopoietic precursor cells (HPCs: CD34+/CD45 dim /VEGFR2−) and endothelial progenitor cells (EPCs: CD34+/CD45−/VEGFR2+) were quantified. Additionally, the effect of mineralocorticoid excess on circulating progenitor cells in normal dogs was studied. The majority of circulating CD34+ cells expressed CD45dimly and did not express VEGFR2, consistent with an HPC phenotype. HPCs were decreased in response to pacing, and this decrease correlated with plasma aldosterone levels (Spearman rank correlation=−0.67, P =0.03). In the hypertensive renal wrap model, administration of DOCA resulted in decreased HPCs. No changes were seen in EPCs in either model. Normal dogs treated with DOCA exhibited a decrease in HPCs in peripheral blood but not bone marrow associated with decreased telomerase activity. Conclusions— This is the first study to demonstrate that mineralocorticoid excess, either endogenous or exogenous, results in reduction in HPCs. These data suggest that mineralocorticoids may induce accelerated senescence of progenitor cells, leading to their reduced survival and decline in numbers.