bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low-energy endocardial defibrillation using an axillary or a pectoral thoracic electrode location.
Authors: Saksena S , DeGroot P , Krol R B , Raju R , Mathew P , Mehra R 
Published: June 2012

BACKGROUND
A significant proportion of patients receiving endocardial defibrillation lead systems must accept either high defibrillation thresholds (DFTs) with lower safety margins or lead implantation by thoracotomy. We examined the feasibility of achieving universal application of endocardial leads and lower defibrillation energy requirements by optimizing the lead system location in conjunction with biphasic shocks.

METHODS AND RESULTS
Two defibrillation catheter electrodes were positioned in the right ventricle and superior vena cava. Thoracic patch electrodes were placed at three sites (apical, pectoral, and axillary). Fifteen-joule, 10-J, and 5-J bidirectional simultaneous biphasic shocks were delivered across three different triple electrode configurations (right ventricle, superior vena cava, and patch) after inducing ventricular fibrillation (VF), and DFT was determined. All patients in whom VF was reproducibly inducible (14 patients) could be reproducibly defibrillated at 15 J at one or more patch electrode locations. Fifteen-joule shocks were effective at three thoracic electrode locations in 12 patients and at two electrode locations in 6 patients. The lowest mean single-shock DFT was 8.1 +/- 3.8 J. In 4 patients, ventricular flutter was reproducibly induced and reverted at 15 J in all patients. Mean DFT for the axillary location was 8.3 +/- 3.5 J and was significantly lower than apical (12.8 +/- 5.6 J, P = .008) and pectoral (11.6 +/- 4.1 J, P < .04) patch locations. The probability of success was significantly higher at 10 J with axillary location (78% of patients, P < .03 compared with both other sites) and at 15 J (P < .05 compared with the apical location). Low-energy endocardial defibrillation (< or = 10 J) was feasible in 10 of 14 tested patients at more than 1 thoracic electrode location at 10 J, whereas only 1 of 7 successful patients could be reverted at more than 1 electrode location at 5 J (P < .02).

CONCLUSIONS
The use of axillary or pectoral patch lead location can allow endocardial defibrillation with biphasic shocks at energies < or = 15 J in this lead configuration. Virtually universal application of endocardial defibrillation lead systems can be predicted from these data. Reduction in maximum pulse generator output to < or = 25 J using these two thoracic electrode locations with bidirectional shocks can be feasible and maintain an adequate safety margin and permit thoracic pulse generator implantation. Lowering endocardial defibrillation energy < 10 J requires increasing specificity of thoracic electrode location.
Electrocardiographic abnormalities and 30-year mortality among white and black men of the Charleston Heart Study.
Authors: Sutherland S E , Gazes P C , Keil J E , Gilbert G E , Knapp R G 
Published: June 2012

BACKGROUND
The long-term predictive significance of a single ECG tracing for mortality was explored among the white and black men of the Charleston Heart Study.

METHODS AND RESULTS
The 1960 baseline tracings of men ages 35 to 74 in the Charleston Heart Study cohort were coded according to the Minnesota classification. Tracings were categorized as being normal or having minor or major abnormalities. The 30-year vital status was ascertained for the cohort, and the association between ECG findings and coronary and all-cause mortality was evaluated. The proportion of black men with major abnormalities at the 1960 baseline examination was almost twice that of white men. Rates of all-cause mortality increased with severity of abnormalities for white and black men. The absolute excess risk for black men with major abnormalities was 23.3 per 1000 person-years and 12.8 for white men. The excess risk for coronary mortality was 7.3 for white men and 6.5 for black men.

CONCLUSIONS
Many of the findings in this study confirm earlier associations derived from studies of white populations and extend the observations to black men. However, the magnitude of the relative risk for mortality was different for white and black men. After controlling for traditional coronary disease risk factors and minor abnormalities, white men with major abnormalities were 2.72 (95% confidence interval, 1.47, 5.04) times more likely to die of coronary disease compared with black men, who were 1.95 (95% confidence interval, 0.93, 4.11) times more likely to die of coronary disease.
Doppler hemodynamic profiles of 82 clinically and echocardiographically normal tricuspid valve prostheses.
Authors: Connolly H M , Miller F A , Taylor C L , Naessens J M , Seward J B , Tajik A J 
Published: June 2012

BACKGROUND
Normal Doppler hemodynamics for tricuspid prostheses have not been well characterized in a large group of patients. Therefore, we analyzed comprehensive Doppler echocardiographic examinations of 82 patients with tricuspid prostheses that were normal by clinical and two-dimensional echocardiographic examinations to establish the normal hemodynamics of various types and sizes of tricuspid prostheses.

METHODS AND RESULTS
The earliest complete postoperative echocardiographic study from each patient was chosen for analysis. Doppler examinations were analyzed on an off-line station from tapes or Doppler strip charts. Early velocity, atrial velocity, end-diastolic velocity, pressure half-time, and mean gradient were obtained by digitizing tricuspid velocity curves. The incidence of "physiological" tricuspid prosthetic regurgitation was noted. Ten Doppler cycles were measured for each patient, and maximal, minimal, and average measurements were recorded. The mean values +/- SD of early velocity, atrial velocity, end-diastolic velocity, mean gradient, and pressure half-time and incidence of mild prosthetic regurgitation were reported for each type of prosthesis, as were highest Doppler measurements for each valve type. Average pressure half-time was significantly lower for St Jude than for heterograft prostheses (P = .04). There were no significant differences between the valve types for mean gradient, early velocity, or incidence of prosthetic regurgitation. Increasing prosthesis size was associated with lower average pressure half-time for heterograft prostheses (P = .024). Average differences (respiratory- and cycle-length-dependent) between maximal and minimal values for 10 cardiac cycles were established for each prosthesis.

CONCLUSIONS
This study establishes normal ranges for Doppler hemodynamics of various tricuspid prostheses and emphasizes the importance of measuring multiple cycles for each tricuspid prosthesis, regardless of cardiac rhythm.
Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland. A paradox.
Authors: Artaud-Wild S M , Connor S L , Sexton G , Connor W E 
Published: June 2012

BACKGROUND
For decades, the coronary heart disease (CHD) mortality rate has been four or more times higher in Finland than in France despite comparable intakes of dietary cholesterol and saturated fat. A potential answer to this paradox is provided by this study of 40 countries and the analyses of other nutrients in the diets besides cholesterol and saturated fat.

METHODS AND RESULTS
CHD death rates for men aged 55 to 64 years were derived from the World Health Organization annual vital statistics. Dietary intakes were gathered from the Food and Agriculture Organization of the United Nations database. Forty countries at various levels of economic development and 40 dietary variables were investigated, including a lipid score that combined the intakes of cholesterol and saturated fat (Cholesterol-Saturated Fat Index [CSI]). The CSI was significantly and positively related to CHD mortality in the 40 countries. The countries with low CSIs had low CHD death rates. Countries with high CSIs had a wide range of CHD death rates. France, Finland, and other Western industrialized countries had similar CSIs. After adjusting for cholesterol and saturated fat, milk and many components of milk (butterfat, milk protein, calcium from milk, and riboflavin) and total calcium remained positively related to CHD mortality for all 40 countries. There were differences in the consumption of these foods and nutrients in France and Finland. Milk and butterfat (fat from milk, cream, cheese, and butter) consumption was higher in Finland than in France. The consumption of plant foods, recently shown to be protective against CHD (vegetables and vegetable oils containing monounsaturated and polyunsaturated fatty acids), was greater in France than in Finland.

CONCLUSIONS
Over the years, France and Finland, with similar intakes of cholesterol and saturated fat, consistently have had very different CHD mortality rates. This paradox may be explained as follows. Given a high intake of cholesterol and saturated fat, the country in which people also consume more plant foods, including small amounts of liquid vegetable oils, and more vegetables (more antioxidants) had lower rates of CHD mortality. On the other hand, milk and butterfat were associated with increased CHD mortality, possibly through their effects on thrombosis as well as on atherosclerosis.
Effect of combined supplementation with alpha-tocopherol, ascorbate, and beta carotene on low-density lipoprotein oxidation.
Authors: Jialal I , Grundy S M 
Published: June 2012

BACKGROUND
Data continue to accumulate supporting a proatherogenic role for oxidized low-density lipoprotein (Ox-LDL). Antioxidant micronutrients such as ascorbate, alpha-tocopherol, and beta carotene, levels of which can be favorably manipulated by dietary measures without side effects, could be a safe approach in inhibiting LDL oxidation. In fact, in vitro studies have shown that all three antioxidants can inhibit LDL oxidation. The present study was undertaken to ascertain both the safety and antioxidant effect of combined supplementation with alpha-tocopherol, ascorbate, and beta carotene on LDL oxidation.

METHODS AND RESULTS
The effect of combined supplementation with alpha-tocopherol (800 IU/d) plus ascorbate (1.0 g/d) and beta carotene (30 mg/d) on copper-catalyzed LDL oxidation was tested in a randomized, placebo-controlled study in two groups of 12 male subjects over a 3-month period. Blood samples for the lipoprotein profile, antioxidant levels, and LDL isolation were obtained at baseline and at 3 months. Neither placebo nor combined antioxidant therapy resulted in any side effects or exerted an adverse effect on the plasma lipoprotein profile. Compared with placebo, combined antioxidant therapy resulted in a significant increase in plasma ascorbate and lipid standardized alpha-tocopherol and beta carotene levels (2.6-, 4.1-, and 16.3-fold, respectively). At baseline, there were no significant differences in the time course curves and kinetics of LDL oxidation as evidenced by the thiobarbituric acid reacting substances (TBARS) assay and the formation of conjugated dienes. However, at 3 months, combined supplementation resulted in a twofold prolongation of the lag phase and a 40% decrease in the oxidation rate. The combined antioxidant group was also compared with a group that received 800 IU of alpha-tocopherol only. Although the combined antioxidant group had significantly higher ascorbate and beta carotene levels than the group supplemented with alpha-tocopherol alone, there were no significant differences between the two groups with respect to LDL oxidation kinetics.

CONCLUSIONS
Combined supplementation with ascorbate, beta carotene, and alpha-tocopherol is not superior to high-dose alpha-tocopherol alone in inhibiting LDL oxidation. Hence, alpha-tocopherol therapy should be favored in future coronary prevention trials involving antioxidants.
Heart disease deaths in a Japanese urban area evaluated by clinical and police records.
Authors: Baba S , Ozawa H , Sakai Y , Terao A , Konishi M , Tatara K 
Published: June 2012

BACKGROUND
By national statistics, Japanese ischemic heart disease (IHD) mortality is one of the lowest of all industrialized countries, and the proportion of deaths due to heart failure in heart disease is the highest. There may be a difference in diagnostic preference between Japan and other industrialized countries.

METHODS AND RESULTS
IHD deaths according to the death certificates were reevaluated with World Health Organization MONICA criteria for those 25 to 74 years old by use of clinical and police records in a Japanese city with a population of 347,000. Their cause of death was given on the death certificates as IHD (International Classification of Diseases [ICD], ninth revision, codes 410-414), heart failure (428), or other heart diseases (393-405, 415-427, 429) in 1984 through 1986. Some deaths in 1985 through 1986 from stroke (430-438) or other diseases (250, 272, 278, 440-448, 797-799) were added. Of 409 subjects, 397 (97%) could be examined. Reevaluation of the 106 deaths originally diagnosed as IHD yielded 73 IHDs and 11 sudden deaths of unknown origin (SD), and reevaluation of 160 deaths originally called heart failure yielded 26 IHDs and 50 SDs. In total, reevaluation of all 397 deaths yielded 101 IHDs and 69 SDs. Some 88% of SD cases were originally certified as heart failure (72%) or IHD (16%). Only two SDs were originally certified as stroke.

CONCLUSIONS
Assuming that 30% of SDs were due to IHD, the number of IHD deaths would be 122, which is 11% larger than the number of IHD deaths according to the death certificates. After reevaluation, the IHD mortality in this study area still was the lowest in the industrialized countries.
Blood pressure modulation by central venous pressure and respiration. Buffering effects of the heart rate reflexes.
Authors: Triedman J K , Saul J P 
Published: June 2012

BACKGROUND
Despite constant fluctuations in cardiac preload caused by the effects of respiration and changes in posture on venous return to the heart, arterial blood pressure remains remarkably constant. The effects of instantaneous lung volume (ILV) and variations of central venous pressure (CVP) on blood pressure (BP) were studied by use of frequency domain techniques to quantify the contribution of heart rate (HR) reflexes to attenuation of the effects of changes in right ventricular preload on arterial pressure.

METHODS AND RESULTS
Random independent variation of ILV, then CVP (obtained using lower-body negative pressure), was performed in eight humans in the supine position. HR, ILV, CVP, and systolic (SBP) and diastolic (DBP) BPs were recorded during control periods and after complete blockade obtained by use of 0.04 mg/kg atropine and 0.2 mg/kg propranolol. A frequency-domain analysis was performed on pairwise relations by the cross-spectral technique. During autonomic blockade, fluctuations in CVP were induced up to 0.14 Hz but caused corresponding changes in arterial pressure only up to 0.08 Hz (P < .02), indicating a mechanical damping effect of the heart and pulmonary vasculature. Fluctuations of BP were also delayed from CVP by 1.55 to 2.10 seconds. At frequencies < 0.1 Hz, relations of CVP to all indices of BP increased with blockade (CVP-SBP, 0.9 +/- 0.5 versus 2.7 +/- 0.8 mm Hg/mm Hg, P < .01; CVP-DBP, 1.3 +/- 0.4 versus 4.3 +/- 1.4 mm Hg/mm Hg, P < .01; CVP-pulse pressure [PP], 1.0 +/- 0.3 versus 1.9 +/- 0.8 mm Hg/mm Hg, P < .05). Higher-frequency fluctuations of arterial BP were a relatively pure manifestation of respiratory activity. At frequencies from 0.15 to 0.35 Hz, the relation of ILV to SBP was unchanged with blockade, whereas relations of ILV to DBP and PP decreased (ILV-DBP, 6.1 +/- 3.5 versus 3.3 +/- 2.2 mm Hg/L, P < .02; ILV-PP, 7.0 +/- 4.3 versus 2.7 +/- 2.2 mm Hg/L, P < .01). An associated change in phase of these relations suggested that neurally mediated changes in HR may offset mechanical effects caused by respiration.

CONCLUSIONS
Both slow changes of BP (< 0.08 Hz) induced by variations of CVP and more rapid changes induced by ILV are actively buffered by heart rate reflexes. During blockade, the mechanical properties of interposed cardiopulmonary structures limit CVP-induced fluctuations of BP. These findings have implications for BP regulation in pathological conditions associated with impairment of HR control.
Evidence for an association between dehydroepiandrosterone sulfate and nonfatal, premature myocardial infarction in males.
Authors: Mitchell L E , Sprecher D L , Borecki I B , Rice T , Laskarzewski P M , Rao D C 
Published: June 2012

BACKGROUND
Several studies indicate that endogenous hormones play a role in the etiology of coronary artery disease, either as independent risk factors or indirectly, via an effect on lipids, lipoproteins, or other heart disease risk factors.

METHODS AND RESULTS
The relation between endogenous hormone levels and premature (< 56-year-old patients) myocardial infarction was assessed in a retrospective study involving 49 male survivors of premature myocardial infarction and 49 age-matched, volunteer male controls. Serum samples were obtained for each subject the morning after a > or = 12-hour fast and frozen at -70 degrees C for subsequent hormonal analysis. Among the male patients, the average duration between the most recent myocardial infarction and blood sampling was 3.4 years (range, 0.7 to 19.2 years). Individuals reporting the use of any medications with the potential to alter lipid, lipoprotein, or hormone levels were excluded from these analyses. Dehydroepiandrosterone sulfate levels were significantly lower in the patients than in the control subjects. This association remained statistically significant even after accounting for the effects of total cholesterol, triglycerides, the ratio of total to high-density lipoprotein (HDL) cholesterol, HDL, apolipoprotein A-I, apolipoprotein A-II, apolipoprotein B, and body mass index. There were no significant differences in the levels of estradiol, testosterone, or free testosterone or the ratio of estradiol to testosterone between patients and control subjects.

CONCLUSIONS
Our conclusions are limited by the retrospective nature of this study. However, these data indicate that serum dehydroepiandrosterone sulfate levels are inversely related to premature myocardial infarction in males and that this association is independent of the effects of several known risk factors for premature myocardial infarction.
Morning increase in ambulatory ischemia in patients with stable coronary artery disease. Importance of physical activity and increased cardiac demand.
Authors: Parker J D , Testa M A , Jimenez A H , Tofler G H , Muller J E , Parker J O , Stone P H 
Published: June 2012

BACKGROUND
The morning increase in asymptomatic ambulatory ischemia may be due to heightened coronary tone, increased physical activity, or both. If ambulatory ischemia is primarily due to physical activity, then alterations in the schedule of physical activity should be reflected in a corresponding alteration in the occurrence of ischemia. This study was designed to examine the relation between activity patterns and the frequency of ambulatory ischemic episodes and the effect of nadolol on these relations.

METHODS AND RESULTS
A double-blind, randomized, placebo-controlled, crossover trial of nadolol versus placebo was performed in 20 patients with stable coronary artery disease. At the end of each 2-week treatment phase, patients were hospitalized for 48 hours. In the hospital, there was a regular activity day (awaken and assume normal activities at 8:00 AM) and a delayed activity day (awaken at 8:00 AM, arise at 10:00 AM, and begin normal activity at noon). Ambulatory ECG monitoring was performed throughout the hospitalization. On the regular activity day, there was a morning increase in heart rate and in the number of ischemic episodes during therapy with placebo that began at 8:00 AM. In contrast, on the delayed activity day, there was a 4-hour phase shift of the increases in heart rate and the increase in ischemic episodes (ie, at noon) corresponding to the onset of physical activities. Therapy with nadolol caused a 50% reduction in the total number of ischemic episodes (129 versus 65, placebo versus nadolol; P < .02). During nadolol therapy, there was no discernible circadian peak in the number of ischemic episodes on either activity day. During placebo treatment, 87% of ischemic episodes were preceded by an increase in heart rate > or = 5 beats per minute. Although nadolol caused a significant reduction in the total number of episodes preceded by a heart rate increase compared with placebo (99 versus 38 episodes, P < .04), this therapy was associated with a significant increase in the number of episodes not associated with a heart rate increase (15 versus 21 episodes, P < .002).

CONCLUSIONS
The morning increase in ambulatory ischemic episodes is due to physical activity patterns. The majority of ischemic episodes are preceded by a heart rate increase, and it is these episodes that are primarily responsible for the morning increase in ischemia. Therapy with nadolol caused a reduction in the total number of ischemic episodes solely by reducing those episodes preceded by a heart rate increase. In contrast, nadolol caused a significant increase in the number of ischemic episodes not associated with a heart rate increase, perhaps in part because it potentiated coronary vasoconstriction.
Evaluation of standard and active compression-decompression CPR in an acute human model of ventricular fibrillation.
Authors: Shultz J J , Coffeen P , Sweeney M , Detloff B , Kehler C , Pineda E , Yakshe P , Adler S W , Chang M , Lurie K G 
Published: June 2012

BACKGROUND
The mechanisms that underlie cardiopulmonary resuscitation (CPR) in humans remain controversial and difficult to study. This report describes a new human model to evaluate CPR during the first 1 to 2 minutes after the onset of ventricular fibrillation (VF). With this model, standard CPR was compared with active compression-decompression (ACD) CPR, a method that uses a handheld suction device to actively compress and actively decompress the chest.

METHODS AND RESULTS
During routine inductions of VF as part of a transvenous lead cardioverter/defibrillator implantation procedure, CPR was performed in 21 patients if the first defibrillation shock failed and until a successful rescue shock was delivered. Compressions during CPR were performed according to American Heart Association guidelines. For ACD CPR, decompression was performed with up to -30 lbs. Radial arterial and right atrial pressures were measured in all patients. Esophageal pressures, intratracheal pressures, or minute ventilation was measured in the last 13 patients. Application of both CPR techniques increased arterial and right atrial pressures. The mean coronary perfusion pressure was increased throughout the entire CPR cycle with ACD CPR (compression, 21.5 +/- 9.0 mm Hg; decompression, 21.9 +/- 8.7 mm Hg) compared with standard CPR (compression, 17.9 +/- 8.2 mm Hg; decompression, 18.5 +/- 6.9 mm Hg; P < .02 and P < .02, respectively). Ventilation per compression-decompression cycle was 97.3 +/- 65.6 mL with standard CPR and 168.4 +/- 68.6 mL with ACD CPR (n = 7, P < .001). Negative inspiratory pressure was -0.8 +/- 4.8 mm Hg with standard CPR and -11.4 +/- 6.3 mm Hg with ACD CPR (n = 6, P < .04).

CONCLUSIONS
Patients undergoing multiple inductions of VF during cardioverter/defibrillator implantation with transvenous leads provide a well-controlled and reproducible model to study the mechanisms of CPR. Using this model, ACD CPR significantly increased arterial blood pressure, coronary perfusion pressure, minute ventilation, and negative inspiratory pressure compared with standard CPR.