bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cigarette smoking and the development and progression of aortic atherosclerosis. A 9-year population-based follow-up study in women.
Authors: Witteman J C , Grobbee D E , Valkenburg H A , van Hemert A M , Stijnen T , Hofman A 
Published: June 2012

BACKGROUND
Cigarette smoking has been recognized as an important risk factor for cardiovascular disease in men and women. Whether the increased risk results from an atherogenic effect of smoking is still debated. We examined the relation between cigarette smoking and atherosclerotic changes in the abdominal aorta.

METHODS AND RESULTS
The association between cigarette smoking and atherosclerotic changes in the abdominal aorta was examined in a population-based cohort of 758 women, initially aged 45 to 64 years. All women were examined radiographically for calcified deposits in the abdominal aorta, which have been shown to represent intimal atherosclerosis. After 9 years of follow-up, atherosclerotic changes, indicating development or progression of plaques, could be demonstrated in 37% of women. A direct association was found between atherosclerotic change and number of cigarettes smoked per day. Compared with women who had never smoked, the relative risks of those who smoked 1 to 9, 10 to 19, and 20 or more cigarettes per day were 1.4 (95% confidence interval, 1.0 to 2.0), 2.0 (1.6 to 2.5), and 2.3 (1.8 to 3.0), respectively, after adjustment for age and other cardiovascular risk factors. Associations of atherosclerotic change with inhaling habit and duration of smoking were borderline significant after number of cigarettes smoked per day was taken into account. Among former smokers, the risk decreased with increasing duration of stopping but a significant excess risk was still observed after 5 to 10 years since quitting (relative risk, 1.6; 95% confidence interval, 1.1 to 2.2).

CONCLUSIONS
These follow-up data support the evidence for an effect of cigarette smoking on atherosclerosis. The findings suggest that the rate of atherosclerotic change may be reduced by cessation of smoking, but a residual effect appears to be present for at least 10 years.
Alcohol consumption and insulin concentrations. Role of insulin in associations of alcohol intake with high-density lipoprotein cholesterol and triglycerides.
Authors: Mayer E J , Newman B , Quesenberry C P , Friedman G D , Selby J V 
Published: June 2012

BACKGROUND
The relation between alcohol intake and insulin levels may explain, in part, the reported associations of alcohol with cardiovascular disease risk factors, including high-density lipoprotein (HDL) cholesterol, triglycerides, blood pressure, and glucose levels, each of which has been recognized as a component of the insulin resistance syndrome.

METHODS AND RESULTS
Subjects included nondiabetic participants of the Kaiser Permanente Women Twins Study (1989 through 1990). Usual alcohol intake was assessed as part of a food frequency questionnaire. For women from twin pairs in which both twins drank (n = 338), an increment of 12 g of alcohol per day (about one drink) was associated with an 8% lower 2-hour post-glucose-load insulin (P < .01) in a multiple regression analysis for twin data, adjusted for age, body mass index, waist-to-hip ratio, total caloric intake, and family history of diabetes. With genetic influences removed by matched analysis of the subset of 98 monozygotic twin pairs, an intrapair difference of 12 g of alcohol per day was associated with a 12.4% intrapair decrement in postload insulin (P < .01). Inverse associations were also seen for fasting insulin. Alcohol consumption was inversely associated with postload glucose but not with fasting glucose in unmatched (P = .05) and matched (P = .005) analyses. A significant positive association of alcohol intake with high-density lipoprotein cholesterol and an inverse relation of alcohol intake with triglycerides were each independent of insulin levels (P < or = .02 in the matched models). Neither systolic nor diastolic blood pressures were related to alcohol consumption in this sample, perhaps because of the rather low level of alcohol intake in the study population (median, 4 g/d).

CONCLUSIONS
Within the range of light to moderate drinking habits, alcohol consumption was inversely related to fasting and postload insulin levels. This relation did not explain associations of alcohol intake with lipid levels and may instead reflect an additional mechanism by which moderate alcohol consumption impacts cardiovascular disease risk.
Impact of regional ventricular function, geometry, and dobutamine stress on quantitative 99mTc-sestamibi defect size.
Authors: Sinusas A J , Shi Q , Vitols P J , Fetterman R C , Maniawski P , Zaret B L , Wackers F J 
Published: June 2012

BACKGROUND
Serial myocardial perfusion imaging with 99mTc-sestamibi (MIBI) was used to evaluate infarct risk area and salvage after thrombolysis. The purpose of this investigation was to determine whether changes in MIBI defect size observed after reperfusion may result in part from distortion of regional and global left ventricular geometry.

METHODS AND RESULTS
Twenty-five open-chest dogs were subjected to either 15 minutes (groups 1A and 1B) or 3 hours (group 2) of left anterior descending coronary artery occlusion followed by 3 hours of reperfusion. MIBI was injected before occlusion (group 1A) or during occlusion (groups 1B and 2), and serial ECG-gated planar imaging was performed. Dobutamine was infused after 3 hours of reperfusion (groups 1B and 2) to transiently alter left ventricular size and function. Perfusion defect magnitude (DM) and extent (DE) were serially quantified with circumferential profile analysis of end-systolic (ES), end-diastolic (ED), and summed images. Flow was assessed with radiolabeled microspheres and correlated with myocardial MIBI activity. Myocardial thickening was assessed in the risk area with sonomicrometers. In group 1A dogs, ischemic dyskinesis produced large artifactual quantitative MIBI defects on ES images (DM, 9.3 +/- 1.3; DE, 27.8 +/- 6.0) that were significantly smaller on ED images (DM, 4.5 +/- 0.9, P < .05; DE, 4.4 +/- 2.3, P < .05). In addition, DM and DE correlated inversely with myocardial thickening on ES images (DM, r = -.84; DE, r = -.78) and summed images (DM, r = -.72; DE, r = -.61) but not ED images (DM, r = -.12; DE, r = -.15). An index of defect reduction derived from summed images correlated well with thickening fraction in stunned dogs (group 1B, r = .89) but poorly in infarcted dogs (group 2, r = .41) subjected to dobutamine stress.

CONCLUSIONS
99mTc-MIBI defect size may be affected by alteration of left ventricular geometry. Changes in regional function may confound analysis of risk area and myocardial salvage with serial 99mTc-MIBI imaging and may also affect defect size during pharmacological stress with dobutamine. Dobutamine 99mTc-MIBI imaging may be useful for distinguishing viable and nonviable myocardium.
Circadian variation of sudden cardiac death reflects age-related variability in ventricular fibrillation.
Authors: Arntz H R , Willich S N , Oeff M , Brüggemann T , Stern R , Heinzmann A , Matenaer B , Schröder R 
Published: June 2012

BACKGROUND
Previous studies report a morning peak in the occurrence of out-of-hospital sudden cardiac death but lack detailed information on underlying arrhythmias. We used the documentation system of the semiautomated defibrillators used by emergency medical technicians to investigate the circadian pattern of defined arrhythmias and the influence of demographic patient characteristics on this pattern.

METHODS AND RESULTS
From December 1988 to December 1990, 703 consecutive patients (63% men; age, 67 +/- 17 years) with sudden cardiac death were registered in the Klinikum Steglitz area of the Berlin emergency care system. Determination of time of day of the event was based on the arrival time of the rescue squad. A marked circadian variation (P < .0001) in the occurrence of sudden cardiac death was observed with a primary morning peak (6 AM to noon) and a secondary afternoon peak (3 to 7 PM). The subgroup of 294 patients with ventricular fibrillation as initially documented arrhythmia showed a similar circadian variation (P < .0001). In significant contrast (P < .01), patients with asystole (n = 260) or pulseless bradyarrhythmias (n = 149) were more evenly distributed during the daytime with a primary night trough. Multivariate logistic regression analysis revealed that the circadian pattern of ventricular fibrillation was similar in both gender groups but tended to differ with regard to age: patients older than 65 years demonstrated a monophasic distribution, whereas patients aged 65 years or less had a biphasic distribution with peaks in the morning and in the afternoon.

CONCLUSIONS
The circadian pattern of sudden cardiac death reflects primarily a circadian variation in onset of ventricular fibrillation. The different circadian patterns of ventricular fibrillation, pulseless bradyarrhythmias, and asystole suggest different pathophysiological mechanisms of causation of death. The age dependence of the pattern of ventricular fibrillation may indicate different underlying external or endogenous triggers.
Myocardial force-frequency defect in mitral regurgitation heart failure is reversed by forskolin.
Authors: Mulieri L A , Leavitt B J , Martin B J , Haeberle J R , Alpert N R 
Published: June 2012

BACKGROUND
Postoperative ejection phase parameters and patient survival rates for mitral valve replacement surgery are considerably lower than for similar aortic valve surgery. While chordal transection probably is the major contributor to the lowered values, there is also evidence for decreased preoperative myocardial contractile reserve in mitral regurgitation patients. This study characterizes abnormalities in the force-frequency relation that may underlie impaired function of myocardium isolated from mitral regurgitation patients with New York Heart Association class II-III heart failure.

METHODS AND RESULTS
Left ventricular epicardial myocardium was obtained by surgical biopsy during mitral valve replacement surgery in patients with mitral regurgitation heart failure (left ventricular ejection fraction, 0.64 +/- 0.05) and during coronary artery bypass surgery in patients with normal ventricular function. The steady-state twitch tension versus frequency relation was measured in myocardial strip preparations (37 degree C, 12 to 228 min-1) in the absence and presence of forskolin. Relative to normal function, peak isometric twitch tension in mitral regurgitation is depressed by 50% (P < .02) and 74% (P < .003) at contraction frequencies of 60 min-1 and 168 min-1, respectively. The slope of the tension-frequency curve is blunted and its peak is shifted to a lower frequency (mitral regurgitation: 134 min-1; normal function: 173 min-1; P < .02). The myosin heavy chain concentration did not differ between mitral regurgitation and normal function strips (53 +/- 4 versus 54 +/- 4 nmol/g blotted wt). Forskolin (0.5 mumol/L) completely reversed the tension depression, blunting, and the lowered peak frequency in the mitral regurgitation preparations.

CONCLUSIONS
Preoperatively, myocardial tension generation in mitral regurgitation patients is severely depressed, and the force-frequency curve is blunted and has a negative slope in the exercise range of heart rates. The reversal of these defects by forskolin suggests that abnormal excitation-contraction coupling may underlie the decreased contractile reserve in mitral regurgitation patients.
Increased aortic impedance precedes peripheral vasoconstriction at the early stage of ventricular failure in the paced canine model.
Authors: Eaton G M , Cody R J , Binkley P F 
Published: June 2012

BACKGROUND
Aortic input impedance is altered in patients with congestive heart failure. However, little is known about whether this vascular response is an early change or a late manifestation of left ventricular dysfunction.

METHODS AND RESULTS
This investigation used a paced canine model of congestive heart failure to demonstrate that abnormal aortic input impedance does evolve in the setting of ventricular systolic dysfunction and to prospectively define the time course of change in aortic input impedance and conduit vessel compliance. Studies were performed in closed-chest conditioned beagles aged 1 to 2 years that underwent hemodynamic evaluation at baseline and after induction of left ventricular dysfunction by rapid ventricular pacing. Within 48 hours of the onset of rapid ventricular pacing, we observed mild left ventricular systolic dysfunction with an echocardiographically derived left ventricular ejection fraction of 37% (p < .001 compared with baseline) measured during interruption of rapid ventricular pacing. Concomitant with this reduction in left ventricular systolic function, the aortic input impedance spectrum was shifted above baseline in all dogs studied. Characteristic impedance of the aorta significantly increased from 121 +/- 65 dynes.s/cm5 to 186 +/- 114 dynes.s/cm5 (P < .02), and a significant increase in the first modulus of impedance from 137 +/- 43 dynes.s/cm5 to 228 +/- 139 dynes.s/cm5 was observed (P < .05). Although characteristic aortic impedance increased by 50%, there was at this point no change in peripheral vascular resistance. Therefore, these abnormalities in aortic input impedance are representative of an early vascular change that evolves in response to ventricular systolic dysfunction.

CONCLUSIONS
Considering the early appearance of these findings, the resultant impaired power transfer and reduced conduit vessel compliance likely contribute to the progression of abnormal myocardial energetics and systolic dysfunction characteristic of ventricular failure.
Selective pulmonary vasodilation by inhaled nitric oxide is due to hemoglobin inactivation.
Authors: Rimar S , Gillis C N 
Published: June 2012

BACKGROUND
Inhaled nitric oxide gas selectively decreases pulmonary artery pressure without affecting systemic arterial pressure. To determine if the selective pulmonary vasodilating effect of inhaled nitric oxide gas is due to inactivation by hemoglobin, we studied the ability of whole blood to inhibit the vasodilator activity of effluent from isolated lungs exposed to inhaled nitric oxide.

METHODS AND RESULTS
The effluent from ventilated, Krebs-perfused rabbit lungs was passed directly over 3- to 4-mm rabbit aortic rings. Inhaled nitric oxide (150 ppm for 3 minutes) reduced pulmonary perfusion pressure, elevated by a continuous infusion of U46619, by 35 +/- 7% (mean +/- SEM, n = 5). Lung effluent from this series of experiments caused 40 +/- 13% relaxation of phenylephrine-preconstricted aortic rings. When blood was added to the combined lung/ring perfusion cascade (final hemoglobin concentration, 1 g/dL), inhaled nitric oxide again significantly reduced pulmonary perfusion pressure, but the effluent now failed to relax the aortic rings (30 +/- 6% [control] versus 1.5 +/- 1% [blood]). Both reduction in pulmonary perfusion pressure and relaxation of the rings during nitric oxide exposure were unchanged from control values after discontinuing the blood infusion.

CONCLUSIONS
The presence of hemoglobin, even in extremely small amounts, restricts the vasodilating effect of inhaled nitric oxide gas to the pulmonary circulation.
Circulating and tissue endothelin immunoreactivity in hypercholesterolemic pigs.
Authors: Lerman A , Webster M W , Chesebro J H , Edwards W D , Wei C M , Fuster V , Burnett J C 
Published: June 2012

BACKGROUND
Hypercholesterolemia is characterized by a coronary vasoconstrictive response to the endothelium-dependent vasodilator acetylcholine. This abnormality may be due to reduced synthesis of endothelium-derived relaxing factor and/or enhanced synthesis and release of an endothelium-derived contracting factor. Endothelin is an endothelium-derived vasoconstrictor and mitogenic peptide that is present in normal plasma, and its circulating concentrations are elevated in disease states that are characterized by abnormal endothelium-dependent relaxation to acetylcholine. The current studies were designed to test the hypotheses that experimental hypercholesterolemia results in elevation of plasma and tissue endothelin immunoreactivity and that the abnormal acetylcholine-evoked coronary vasoconstriction in the hypercholesterolemic animals is associated with further elevation of plasma endothelin.

METHODS AND RESULTS
Plasma concentrations and molecular forms of endothelin immunoreactivity were determined following 2% cholesterol diet for 4 months in pigs and during intracoronary acetylcholine administration. Second, we assessed the presence of endothelin in the coronary vascular wall by using immunohistochemistry. Hypercholesterolemia elevated plasma endothelin concentration and enhanced coronary artery tissue endothelin immunoreactivity. The endothelium-dependent vasodilator acetylcholine further increases plasma endothelin in hypercholesterolemia in association with coronary vasoconstriction. The predominant molecular form of endothelin in hypercholesterolemia is the biological active endothelin-1.

CONCLUSIONS
This study suggests a role for endothelin as an early participant and a marker for the endothelial dysfunction in hypercholesterolemia as well as a participant in the atherogenic process.
Pressure recovery in aortic valve stenosis.
Authors: Laskey W K , Kussmaul W G 
Published: June 2012

BACKGROUND
Pressure recovery is the variable increase in lateral pressure downstream from a stenotic orifice. The magnitude and clinical significance of pressure recovery in aortic valve stenosis are poorly defined.

METHODS AND RESULTS
We obtained high-fidelity pressure and velocity recordings in 11 patients with isolated significant aortic valve stenosis at the time of diagnostic cardiac catheterization. Systematic catheter pullback from the left ventricular cavity revealed a consistent although variable subvalvular gradient. Further pullback across and distal to the region of the stenosed aortic valve revealed a consistent and progressive increase in the ascending aortic pressure. This increase in lateral pressure occurred pari passu with a diminution in amplitude of the velocity pulse. The extent of pressure recovery was directly related to systemic blood flow and transvalvular flow but inversely related to the Gorlin-derived aortic valve area.

CONCLUSIONS
These findings have potentially important implications for the hemodynamic evaluation of mild to moderately severe aortic valve stenosis. The extent of pressure recovery may be of additional utility in the assessment of aortic valve stenosis under varying physiological states.
Asymptomatic arrhythmias in patients with symptomatic paroxysmal atrial fibrillation and paroxysmal supraventricular tachycardia.
Authors: Page R L , Wilkinson W E , Clair W K , McCarthy E A , Pritchett E L 
Published: June 2012

BACKGROUND
Paroxysmal atrial fibrillation and paroxysmal supraventricular tachycardia are recognized clinically when patients seek treatment for symptoms due to recurrent arrhythmias; atrial fibrillation also increases the risk of stroke. The frequency with which asymptomatic arrhythmias occur in patients with these arrhythmias is unknown.

METHODS AND RESULTS
Twenty-two patients with paroxysmal atrial fibrillation (n = 8) or paroxysmal supraventricular tachycardia (n = 14) were studied for 29 days with two different ambulatory ECG-monitoring techniques to measure the relative frequency of asymptomatic and symptomatic arrhythmias. All class I antiarrhythmic drugs, calcium channel blockers, beta-blockers, and digitalis were withheld. Sustained asymptomatic arrhythmia events (defined as lasting at least 30 seconds) were documented using continuous ambulatory ECG monitoring once weekly for a total of 5 of the 29 study days; symptomatic arrhythmia events were documented using transtelephonic ECG monitoring for all 29 days of the study. In the group of patients with paroxysmal atrial fibrillation, asymptomatic arrhythmia events occurred significantly more frequently than symptomatic arrhythmia events; the mean rates, expressed as events/100 d/patient (95% confidence interval), were 62.5 (40.4, 87.3) and 5.2 (2.7, 9.0) (P < .01); the ratio of the mean rates was 12.1 (5.8, 26.4). In contrast, in the group of patients with paroxysmal supraventricular tachycardia, asymptomatic arrhythmia events were significantly less frequent than symptomatic arrhythmia events; the mean rates were 0.0 (0.0, 5.3) and 7.4 (5.0, 10.6) (P = .02). The ratio of the mean rates was 0.0 (0.0, 0.8).

CONCLUSIONS
In a group of patients with paroxysmal atrial fibrillation, sustained asymptomatic atrial fibrillation occurs far more frequently than symptomatic atrial fibrillation. However, it is not known whether asymptomatic atrial fibrillation is a potential risk factor for stroke even when patients are not having symptomatic arrhythmias.
Pulmonary atresia with ventricular septal defect in adults.
Authors: Marelli A J , Perloff J K , Child J S , Laks H 
Published: June 2012

BACKGROUND
Multistage surgery culminating in completed hemodynamic repair is now performed for pulmonary atresia with ventricular septal defect (PA-VSD). Justification for operation in patients with an adequate collateral pulmonary circulation is controversial. Data on natural adult survival are scant but are necessary to provide the rationale for multistage reconstructive procedures.

METHODS AND RESULTS
All cyanotic adults with PA-VSD in the UCLA Adult Congenital Heart Disease Center Registry from 1978 through 1992 formed the basis for this study. Registry data and echocardiographic, hemodynamic, and angiographic information were used to determine longevity, clinical course, and operative feasibility. Of 26 patients, 16 were unoperated when referred (group A), and 10 had been palliated before age 18 years (group B). Two thirds were 18 to 29 years old. Only 2 patients survived beyond age 40 years. Six died during follow-up at a mean age of 31 years (+/- 12.1 SD). Eight group A patients were in New York Heart Association class II, and 8 were in class III. Of the 26 group A and B patients, 20 had aortic regurgitation, which was moderate or severe in 10. Eight had cardiac failure. Of 11 group A patients who remained unoperated, 5 died. Twelve patients were considered eligible for surgery at > or = 18 years of age. Ten underwent completed hemodynamic repair with a mean post-operative right ventricular-to-left ventricular systolic pressure ratio of 0.45 (+/- 0.16 SD), and there were no early or late deaths.

CONCLUSIONS
Even when collateral blood flow permits adult survival, all such patients are symptomatic. Mean life expectancy without operation did not exceed three decades. Aortic regurgitation and cardiac failure are significant negative variables. Nearly half of unoperated adults died during follow-up. Staged hemodynamic repair can be performed with a low surgical risk in properly selected adults with PA/VSD.