bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantitative Doppler assessment of valvular regurgitation.
Authors: Enriquez-Sarano M , Bailey K R , Seward J B , Tajik A J , Krohn M J , Mays J M 
Published: June 2012

BACKGROUND
Quantitation of valvular regurgitation remains a challenge. The accuracy of quantitative Doppler is controversial, and its ability to measure regurgitant volume is unknown; therefore, it is not widely used.

METHODS AND RESULTS
In 120 patients (20 without regurgitation, 19 with aortic regurgitation, and 81 with mitral regurgitation), the stroke volume through the mitral annulus and left ventricular outflow tract were measured using pulsed-wave Doppler concurrently with left ventricular stroke volume calculated using left ventricular volumes measured by two-dimensional echocardiography Simpson's biapical method. Regurgitant volume and fraction were thus computed using Doppler or ventricular methods. In normal patients there were good correlations between Doppler and left ventricular measurements of stroke volume. Doppler regurgitant volume and fraction were 4.4 +/- 4.4 mL and 5.3 +/- 4.5%, respectively. In patients with aortic regurgitation, there were good correlations between Doppler and left ventricular measurements of stroke volume, regurgitant volume, and regurgitant fraction (r = 0.97, r = 0.95, and r = 0.93, respectively; p < 0.0001). In patients with mitral regurgitation, despite good correlations between Doppler and ventricular methods for stroke volume, regurgitant volume, and regurgitant fraction (r = 0.94, r = 0.93, and r = 0.94, respectively; p < 0.001), these variables were overestimated by Doppler. However, in the last 54 patients compared with the first 27, overestimation decreased significantly for regurgitant volume (5 +/- 10 mL versus 18 +/- 27 mL, p < 0.05) and regurgitant fraction (3.3 +/- 6.7% versus 6.2 +/- 6.8%, p = 0.05).

CONCLUSIONS
Quantitative Doppler can be performed in large numbers of patients in a clinical laboratory. Its potential limitation was identified as overestimation of mitral regurgitation, which is overcome with increased experience. Its achieved accuracy in mitral and aortic regurgitation allows measurement not only of regurgitant fraction but most importantly of regurgitant volume.
Electrophysiological effects of high cocaine concentrations on intact canine heart. Evidence for modulation by both heart rate and autonomic nervous system.
Authors: Clarkson C W , Chang C , Stolfi A , George W J , Yamasaki S , Pickoff A S 
Published: June 2012

BACKGROUND
Previous clinical reports have suggested that cocaine intoxication may produce severe ventricular arrhythmias due to a direct effect on the heart. However, the effects of high plasma levels of cocaine on the electrophysiology of the heart have not been well characterized and remain poorly understood.

METHODS AND RESULTS
The purpose of this study was to characterize the electrophysiological effects of high doses of cocaine on the in situ dog heart. In dogs anesthetized with morphine and alpha-chloralose, cocaine (2-11 micrograms/mL) increased both atrial and ventricular refractory periods and produced rate-dependent increases in atrial, atrioventricular, His-Purkinje, and ventricular conduction intervals. The time constant for the onset of cocaine's conduction slowing effect following a reduction in pacing cycle length from 400 to 260 msec was approximately two beats, and the time constant for diastolic recovery from conduction slowing was approximately 200 msec, which are similar to values reported for several class Ib antiarrhythmic drugs. Cocaine produced a rate-dependent increase in QT interval that was greatest at high heart rates yet produced no change in the ST (QT-QRS) interval. This suggests that high plasma levels of cocaine delay repolarization primarily via slowing of conduction. Cocaine's effects on both atrioventricular and intraventricular conduction were significantly larger in autonomically blocked than in autonomically intact animals.

CONCLUSIONS
We conclude that high plasma levels of cocaine, similar to those reported in autopsy reports following fatal cocaine overdose in humans, produce significant rate-dependent conduction slowing effects on atrial, atrioventricular, and ventricular conduction in the in situ heart. These rate-dependent effects are intensified following autonomic blockade.
Beneficial effect of carnitine on mechanical recovery of rat hearts reperfused after a transient period of global ischemia is accompanied by a stimulation of glucose oxidation.
Authors: Broderick T L , Quinney H A , Barker C C , Lopaschuk G D 
Published: June 2012

BACKGROUND
We have previously shown that increasing myocardial carnitine levels in fatty acid-perfused isolated working rat hearts dramatically increases glucose oxidation rates. Since high levels of fatty acids depress reperfusion recovery of ischemic hearts by inhibiting glucose oxidation, we determined what effect carnitine has on glucose oxidation during reperfusion of ischemic hearts.

METHODS AND RESULTS
Isolated working rat hearts were perfused with 11 mM [5-3H/ul-14C]glucose, 1.2 mM palmitate, and 100 microU/ml insulin and subjected to a 35-minute period of global ischemia followed by aerobic reperfusion. Rates of glycolysis and glucose oxidation were determined by measuring tritiated water and 14CO2 production, respectively. Before ischemia, myocardial carnitine content was first increased by perfusing hearts during a 60-minute baseline aerobic perfusion with 10 mM L-carnitine. This resulted in a significant increase in total myocardial carnitine from 4,804 +/- 358 to 9,692 +/- 2,090 nmol/g dry wt (mean +/- SD). Glycolysis rates in carnitine-treated hearts were not significantly altered compared with control hearts during the aerobic perfusion (2,482 +/- 1,173 versus 1,840 +/- 1,365 nmol glucose.g dry wt-1 x min-1, respectively). In contrast, glucose oxidation rates in carnitine-treated hearts were significantly increased before ischemia compared with control hearts (471 +/- 209 versus 158 +/- 75 nmol glucose.g dry wt-1 x min-1, respectively). During reperfusion of previously ischemic hearts, glycolytic rates returned to preischemic values in both carnitine-treated and control hearts. Glucose oxidation rates also recovered to preischemic values in these hearts and remained significantly elevated in carnitine-treated hearts compared with control hearts (283 +/- 113 versus 130 +/- 27 nmol glucose.g dry wt-1 x min-1, respectively). Mechanical recovery in control hearts returned to 44% of preischemic values (measured as heart rate-peak systolic pressure product), whereas in carnitine-treated hearts, mechanical recovery returned to 71% of preischemic values.

CONCLUSIONS
These results suggest that the beneficial effects of carnitine in the ischemic heart can be explained by the actions of this compound on overcoming fatty acid inhibition of glucose oxidation.
Effects of captopril on ischemia and dysfunction of the left ventricle after myocardial infarction.
Authors: Søgaard P , Gøtzsche C O , Ravkilde J , Thygesen K 
Published: June 2012

BACKGROUND
Treatment with angiotensin converting enzyme inhibitors has been shown to be beneficial in patients with heart failure and myocardial infarction. Experimental studies have shown beneficial effects on the ischemic myocardium.

METHODS AND RESULTS
The effects of captopril were evaluated in 64 patients with left ventricular dysfunction after myocardial infarction. The patients were randomized at day 7 to either placebo or captopril (50 mg daily) in a double-blind parallel study over a period of 6 months. The patients were followed up by means of ambulatory ECG monitoring, bicycle ergometer testing, and echocardiographic examination. The duration of ST segment depression detected during ambulatory ECG monitoring was lower in the captopril group (87 minutes) than in the placebo group (638 minutes) (p < 0.001), and the number of patients in the captopril group with exercise-induced ST segment depression (p < 0.01) was lower at the completion of the study. The working capacity increased during the study period from 540 +/- 47 seconds to 738 +/- 41 seconds (p < 0.01) in the captopril group and was higher than that in the placebo group (530 +/- 43 seconds, p < 0.01) at the end of the study. Furthermore, a significant dilation of the left ventricular end-diastolic and end-systolic volumes was observed in the placebo group (p < 0.05); this was prevented in the captopril group where, in addition, a reduction in end-systolic volume was observed (p < 0.05).

CONCLUSIONS
Captopril has a favorable effect on the dysfunctioning myocardium after myocardial infarction inasmuch as the ischemic burden is reduced, the working capacity is increased, dilation of the left ventricle is prevented, and systolic function is improved.
Effects of age, sex, and menopausal status on plasma lipoprotein(a) levels. The Framingham Offspring Study.
Authors: Jenner J L , Ordovas J M , Lamon-Fava S , Schaefer M M , Wilson P W , Castelli W P , Schaefer E J 
Published: June 2012

BACKGROUND
Lipoprotein(a) [Lp(a)] is an atherogenic particle that structurally resembles a low density lipoprotein (LDL) particle but contains a molecule of apolipoprotein(a) attached to apolipoprotein B-100 by a disulfide bond. Because elevated plasma levels of Lp(a) have been shown to be an independent risk factor for coronary artery disease, it is important to define normal ranges for this lipoprotein.

METHODS AND RESULTS
We have measured Lp(a) in 1,284 men (mean age, 48 +/- 10 years) and 1,394 women (mean age, 48 +/- 10 years) free of cardiovascular and cerebrovascular disease and not on medications known to affect lipids who were seen at the third examination cycle of the Framingham Offspring Study. Plasma Lp(a) levels were measured by an enzyme-linked immunosorbent assay, which uses a "capture" monoclonal anti-apo(a) antibody that does not cross-react with plasminogen, and a polyclonal anti-apo(a) antibody conjugated to horseradish peroxidase. The assay was calibrated to total Lp(a) mass. The Lp(a) frequency distribution was highly skewed to the right, with 56% of the values in the 0-10-mg/dL range. Mean plasma Lp(a) concentrations were 14 +/- 17 mg/dL in men and 15 +/- 17 mg/dL in women. Values of more than 38 mg/dL were above the 90th percentile and values of more than 22 mg/dL were above the 75th percentile in both men and women.

CONCLUSIONS
We have determined mean Lp(a) levels for men and women participating in the Framingham Offspring Study. In this population, there was an inverse association between plasma levels of Lp(a) and triglycerides for both sexes (p < 0.006), but triglycerides accounted for only approximately 0.5% of the variation in Lp(a) levels. Associations of Lp(a) levels with total and LDL cholesterol levels were not significant after correction for the estimated contribution of Lp(a) cholesterol to total and LDL cholesterol. After controlling for age, Lp(a) values were 8% greater in postmenopausal women than in premenopausal women, but this difference was not statistically significant. Body mass index, alcohol consumption, cigarette smoking, use of beta-blockers or cholesterol-lowering medications, and use of drugs for the treatment of diabetes and hypertension were not correlated with Lp(a) levels.
Assessment of the human splanchnic venous volume-pressure relation using radionuclide plethysmography. Effect of nitroglycerin.
Authors: Manyari D E , Wang Z , Cohen J , Tyberg J V 
Published: June 2012

BACKGROUND
No method exists to assess human splanchnic venous function, the most important region in terms of vascular capacity.

METHODS AND RESULTS
We studied 25 stable patients without heart failure or hypertension to develop a method to assess the splanchnic venous volume-pressure (V-P) relation and to determine the effect of nitroglycerin (GTN). We used blood pool scintigraphy to assess changes in regional splanchnic vascular volume (SVV) and low levels of continuous positive airway pressure (CPAP) to passively alter venous pressure and thus, SVV. We postulated that the relation between SVV and the CPAP used would reflect the capacitance of the splanchnic venous bed and that changes in the position of this relation would provide a relative measurement of any change in capacitance. In 12 patients (group 1), the splanchnic vascular V-P curves were recorded before and 2, 9, and 20 minutes after 0.6 mg sublingual GTN; in eight patients (group 2), recordings were made at similar times before and after sublingual administration of placebo; in five patients (group 3), the hemodynamic effects of CPAP were assessed by means of right and left cardiac catheterization. Right atrial and femoral venous pressures increased (p < 0.001) and cardiac output fell (p < 0.05) during CPAP. There was an apparently linear relation between CPAP and SVV (r = 0.74-0.98); SVV increased an average of 7.4 +/- 2.2% (p < 0.001) by 12 cm H2O CPAP: The splanchnic vascular V-P curves were reproducible with minimal variability in SVV (+/- 2%, p > 0.2) in group 2. After administration of GTN, the splanchnic vascular V-P curve shifted away from the pressure axis in a parallel fashion by an average of 9.4 +/- 5.4% (p < 0.001).

CONCLUSIONS
We have developed a reproducible noninvasive technique that may be used to assess human splanchnic venous V-P relations. We have demonstrated for the first time in humans that GTN exerts its dilatory effect by increasing the unstressed splanchnic venous volume.
Quantitative adenosine 201Tl single-photon emission computed tomography for the early assessment of patients surviving acute myocardial infarction.
Authors: Mahmarian J J , Pratt C M , Nishimura S , Abreu A , Verani M S 
Published: June 2012

BACKGROUND
We prospectively investigated whether adenosine 201Tl tomography (SPECT) could determine the extent of coronary artery disease, the presence of jeopardized myocardium, and the risk for in-hospital cardiac events in 120 clinically stable patients early (5 +/- 3 days) after myocardial infarction.

METHODS AND RESULTS
All patients had coronary angiography and SPECT in close proximity. Adenosine SPECT identified 99% of infarct-related arteries and 82% of severely stenosed (> or = 70%) noninfarct arteries. Multivessel disease was accurately predicted in 69% of patients. Sixty-five percent of stenosed noninfarct arteries had matching thallium perfusion defects, and 92% of these were reversible. The specificity of adenosine SPECT was > 90%. Thallium redistribution occurred often within infarct (59%) and noninfarct (92%) zones. The patency status of the arteries, however, did not predict the presence or extent of jeopardized myocardium. The perfusion defect size was larger (p = 0.0001) in patients with (45 +/- 18%) than in those without (22 +/- 15%) in-hospital cardiac events. Furthermore, 90% of patients with events had a > or = 20% perfusion defect compared with only 38% of those without events (p = 0.0001). The positive-predictive accuracy for developing a cardiac event was 70% when the perfusion defect size was > 30%. The ischemic defect also was larger in patients with (19 +/- 14%) than in those without (10 +/- 10%) events (p = 0.001). The positive- and negative-predictive values for developing early postinfarction angina were 43% and 91%, respectively, when the ischemic defect was > 12%.

CONCLUSIONS
In selected low-risk survivors of myocardial infarction, early quantitative adenosine SPECT is safe and accurate in detecting and localizing coronary stenoses, assessing the extent of jeopardized myocardium, and determining subsequent risk for in-hospital cardiac events.
Comparison of resetting and entrainment of uniform sustained ventricular tachycardia. Further insights into the characteristics of the excitable gap.
Authors: Callans D J , Hook B G , Josephson M E 
Published: June 2012

BACKGROUND
Resetting and entrainment have both been used to characterize the electrophysiological properties of the reentrant circuit in ventricular tachycardia. Several entrainment studies have suggested that the circuit has decremental properties, because the return cycle increases at faster pacing rates. Resetting, however, demonstrates a fully excitable gap in the majority of tachycardias.

METHODS AND RESULTS
The response to resetting and overdrive pacing was analyzed in 18 ventricular tachycardias. Resetting demonstrated some duration of a fully excitable gap in 14 of 18 tachycardias. Overdrive pacing was performed at several cycle lengths with an incremental number of stimuli (1-15 beats) such that the first beat that interacted with the tachycardia (the nth beat) could be identified. The return cycles measured during resetting and the nth beat of pacing were identical (r = 0.99). At relatively long paced cycle lengths, paced beats after the nth beat resulted in a constant return cycle in most tachycardias with a fully excitable gap. At rapid paced cycle lengths, an increase in the return cycle from the nth to the nth + 1 beat was associated with progressive prolongation in the return cycle with each incremental paced beat until a longer equilibrium return cycle was reached or the tachycardia terminated in response to pacing.

CONCLUSIONS
We propose that the responses to resetting and overdrive pacing with or without entrainment appear to provide conflicting information about the characteristics of the circuit because they in fact measure entirely different electrophysiological parameters. The nth beat of pacing foreshortens the excitable gap to the extent that it arrives prematurely. Subsequent paced beats interact with an altered tachycardia circuit that has had less time to recover excitability. Resetting is the interaction of a single paced beat with the tachycardia and, as such, provides a more accurate assessment of the characteristics of the unaltered tachycardia circuit.
Does obesity influence early target organ damage in hypertensive patients?
Authors: Schmieder R E , Messerli F H 
Published: June 2012

BACKGROUND
Various prospective studies have found that lean hypertensive patients have greater cardiovascular morbidity and mortality than obese hypertensive subjects. It was therefore hypothesized that hypertension is more benign when associated with obesity. In the present study, we evaluated effects of obesity on early target organ damage in patients with essential hypertension.

METHODS AND RESULTS
In a total of 207 subjects, systemic and renal hemodynamics as well as left ventricular structure and function were assessed by measuring cardiac output (indocyanine green dye dilution), renal blood flow (clearance of 131I paraimmunohippuric acid), and mean arterial pressure (invasively) and by two-dimensionally guided M-mode echocardiographic findings. Systemic and renal vascular resistance, compliance of the large arteries evaluated by the stroke volume/pulse pressure index, and left ventricular mass served as parameters for early target organ damage. All individuals were categorized into four groups: lean and obese normotensive as well as lean and obese hypertensive subjects. In obese hypertensive patients, total peripheral resistance was significantly lower and stroke volume/pulse pressure index was higher than in the lean hypertensive group, almost reaching values of normotensive control subjects. No effect of obesity on the renal circulation was noted, whereas in hypertension, renal vascular resistance was elevated. The degree of left ventricular hypertrophy was more pronounced in the hypertensive groups than in their normotensive counterparts and progressively increased with obesity. Nevertheless, in obese hypertensive patients, left ventricular function, as measured by fractional fiber shortening and velocity of circumferential fiber shortening, was maintained despite the fact that the heart had been exposed to the double burden of an increased preload (obesity) and afterload (hypertension).

CONCLUSIONS
Obesity had a disparate effect on target organs in hypertension. At rest, obesity seemed to mitigate cardiovascular changes in the systemic vascular bed caused by hypertension. However, no such mitigation was observed in the renal vasculature, and left ventricular hypertrophy was even exacerbated by the presence of obesity. Our findings in part negate the concept that obesity is able to exert a protective effect on early target organ damage in hypertensive patients and, in particular, on the heart.
Time course of restenosis during the first year after emergency coronary stenting.
Authors: Kastrati A , Schömig A , Dietz R , Neumann F J , Richardt G 
Published: June 2012

BACKGROUND
Prevention of abrupt vessel closure after percutaneous transluminal coronary angioplasty (PTCA) represents one of the current indications for intracoronary stent implantation. After the procedure, the stented segment undergoes luminal changes that may lead to late restenosis. This study was undertaken to assess the time course of luminal changes during the first year after emergency placement of coronary stents.

METHODS AND RESULTS
Coronary stenting was indicated in patients with present or threatened vessel closure secondary to large dissections after PTCA. From June 1989 to May 1991, 82 patients who received Palmaz-Schatz stents and did not have early vessel occlusion after stenting were enrolled into a serial angiographic follow-up study. Coronary normal reference diameter and minimal luminal diameter were measured with an automated edge detection technique. Patients who underwent repeat PTCA for restenosis were excluded from further serial angiography. The restudy rate at 3, 6, and 12 months was 96%, 81%, and 90% of the eligible patients, respectively. The incidence of restenosis (defined as a diameter stenosis > or = 50%) was 22.0% at 3 months, 31.9% at 6 months, and 33.2% at 12 months. Minimal luminal diameter was increased from 0.66 +/- 0.32 mm before to 2.85 +/- 0.43 mm immediately after stenting. It was 0.46 +/- 0.31 mm smaller than the diameter of the maximally inflated balloon during the procedure. The reduction in minimal luminal diameter was 0.80 +/- 0.69 mm (p = 0.0001) for the first 3 months, 0.29 +/- 0.52 mm (p = 0.0001) between 3 and 6 months, and 0.13 +/- 0.32 mm (p = 0.01) for the last 6 months. The percentage of patients who presented a significant change in minimal luminal diameter (defined as > 0.60 mm) declined from 50.6% during the first 3 months and 18.9% between 3 and 6 months to 6.5% for the period between 6 and 12 months.

CONCLUSIONS
The incidence and the time course of restenosis after emergency coronary stenting are similar to that reported for conventional PTCA. Coronary lumen dimensions demonstrated a peak change at 3 months and remained mostly stable after the first 6 months.