bluuebunny/crossref_metadata_2025 huggingface dataset:
Alterations of heart rate and of heart rate variability after radiofrequency catheter ablation of supraventricular tachycardia. Delineation of parasympathetic pathways in the human heart.
Authors: Kocovic D Z , Harada T , Shea J B , Soroff D , Friedman P L
Published: June 2012

BACKGROUND

Persistent inappropriate sinus tachycardia has been reported as a complication after radiofrequency (RF) ablation of the fast atrioventricular (AV) nodal pathway. The purpose of this study was to evaluate the prevalence of this complication and its mechanism using heart rate variability analysis.

METHODS AND RESULTS

Time and frequency domain analysis of heart rate was performed in the electrophysiology laboratory immediately before and immediately after RF ablation in 64 patients with supraventricular tachycardia. Ablation targets in these 64 patients included the fast AV nodal pathway (n = 3), the slow AV nodal pathway (n = 14), a posteroseptal accessory pathway (n = 23), and a left lateral accessory pathway (n = 24). A control group of 21 patients undergoing diagnostic study but not ablation underwent identical analysis immediately before and at the conclusion of their procedure. Patients undergoing ablation also had time and frequency domain analysis performed on ambulatory 24-hour Holter tapes recorded before ablation and at 1 day, 1 month, and 6 months after ablation. Compared with preablation values, time domain analysis immediately after ablation revealed a significant increase in mean heart rate and significant reductions in heart rate variability expressed as SD, MSSD, and PNN50 in patients undergoing AV nodal modification or posteroseptal accessory pathway ablation. Frequency domain analysis revealed marked attenuation of high frequency (0.15 to 0.40 Hz) components, indicating parasympathetic denervation. These acute changes were not seen after ablation of left lateral accessory pathways or after diagnostic study without ablation. Time and frequency domain analysis of 24-hour ambulatory Holter monitors performed serially after ablation revealed resolution of abnormalities of heart rate and of heart rate variability 1 to 6 months after ablation, with reappearance of the high frequency parasympathetic component suggestive of reinnervation.

CONCLUSIONS

RF ablation in the anterior, mid, and posterior regions of the low interatrial septum may disrupt preganglionic or postganglionic parasympathetic fibers located in these regions that are destined to innervate the sinus node. Such fibers become more scarce along the left AV groove with increasing distance from the posteroseptal space. Parasympathetic denervation may be one mechanism for persistent inappropriate sinus tachycardia after RF ablation.
Cellular electrophysiological effects of hyperthermia on isolated guinea pig papillary muscle. Implications for catheter ablation.
Authors: Nath S , Lynch C , Whayne J G , Haines D E
Published: June 2012

BACKGROUND

The primary mechanism of tissue injury by radiofrequency catheter ablation is presumed to be thermally mediated. However, the myocardial cellular electrophysiological effects of hyperthermia are not well characterized. We used an in vitro model of isolated guinea pig right ventricular papillary muscle to investigate the acute cellular electrophysiological effects of hyperthermia.

METHODS AND RESULTS

Excised guinea pig right ventricular papillary muscles were pinned in a high-flow tissue bath and superfused with Tyrode's solution at 37.0 +/- 0.5 degrees C. The superfusate temperature was rapidly changed to 38.0 to 56.0 degrees C for 60 seconds and then returned to 37.0 degrees C. Conventional microelectrodes were used to measure membrane potential (Vm), maximum rate of rise of the action potential (dV/dtmax), and action potential (AP) amplitude and AP duration at 50% (APD50) and 90% (APD90) repolarization. Hyperthermia resulted in (1) a progressive depolarization of Vm at temperatures > or = 40.0 degrees C, which became more prominent at temperatures > or = 45.0 degrees C; (2) changes in the AP characterized by a temperature-dependent increase in dV/dtmax and a temperature-dependent decrease in AP amplitude, APD50, and APD90; (3) reversible loss of cellular excitability within a temperature range of 42.7 to 51.3 degrees C (median, 48.0 degrees C); (4) irreversible loss of cellular excitability and tissue injury at temperatures > or = 50.0 degrees C; and (5) the development of abnormal automaticity at temperatures > 45.0 degrees C.

CONCLUSIONS

Hyperthermia causes significant changes in myocardial cellular electrophysiological properties that include membrane depolarization, reversible and irreversible loss of excitability, and abnormal automaticity. There appear to be specific temperature ranges for reversible and irreversible electrophysiological changes. These observations may have important implications for tissue temperature monitoring during radiofrequency catheter ablation.
Electrophysiological mechanisms in a canine model of erythromycin-associated long QT syndrome.
Authors: Rubart M , Pressler M L , Pride H P , Zipes D P
Published: June 2012

BACKGROUND

Erythromycin is known to prolong ventricular repolarization and has been associated with the occurrence of torsades de pointes. In this study, we have investigated potential mechanisms in vivo and in vitro for induction of an acquired long QT syndrome by erythromycin.

METHODS AND RESULTS

Ventricular electrograms and endocardial monophasic action potentials were recorded in anesthetized open-chest dogs before and after administration of 40 to 120 mg/kg of erythromycin lactobionate. Conventional microelectrode techniques were used to record transmembrane action potentials in isolated dog Purkinje fibers and papillary muscles. Erythromycin at concentrations > 20 mg/L prolonged action potential duration. At higher concentrations (100 to 200 mg/L), erythromycin induced phase 2 and phase 3 early afterdepolarizations (EADs) both in vivo and in vitro. The effects of erythromycin on repolarization were more marked in Purkinje fibers than in papillary muscle. Pretreatment of Purkinje fibers with erythromycin antagonized the effects of dofetilide, a selective delayed-rectifier potassium channel (IK) blocker. Pretreatment with prazosin or tetrodotoxin had no effect on erythromycin-induced changes in action potential duration.

CONCLUSIONS

These pharmacological studies suggest that erythromycin prolongs repolarization to a large extent by block of IK. In turn, prolongation of action potential duration resulting from erythromycin's actions on IK may promote the development of EADs. The induction of ventricular arrhythmias observed clinically after exposure to erythromycin may be related to the development of EADs. The rarity of occurrence of ventricular arrhythmias suggests that other predisposing factors contribute to the acquired long QT syndrome associated with erythromycin.
Diminished contractile response to increased heart rate in intact human left ventricular hypertrophy. Systolic versus diastolic determinants.
Authors: Liu C P , Ting C T , Lawrence W , Maughan W L , Chang M S , Kass D A
Published: June 2012

BACKGROUND

Experimental studies indicate that in addition to diastolic dysfunction, hypertrophied myocardium can display depressed contractile responses, particularly at rapid heart rates, compounding reserve limitations. This study tests whether such abnormalities exist in intact human subjects at physiological paced rates and, if so, whether they are linked to simultaneous rate-dependent deterioration in diastolic function.

METHODS AND RESULTS

Ten subjects with left ventricular hypertrophy (LVH) and 8 normal control subjects were studied. Most LVH patients presented with dyspnea and/or pulmonary edema and had concentric hypertrophy. Since rapid pacing simultaneously alters cardiac filling volumes and pressures, pressure-volume relation analysis was used to better define changes in contractile response. Patients were instrumented with a conductance catheter and micromanometer for pressure-volume data recording and a balloon occluder at the right atrial-inferior vena caval junction to vary filling and thus generate function relations. Data were obtained at baseline and at three atrial pacing rates (100, 120, 150 min-1). In addition, single-beat force-interval data were used to indirectly examine calcium cycling kinetics. LVH subjects demonstrated baseline diastolic abnormalities, including prolonged relaxation, elevated end-diastolic pressure, and reduced chamber compliance. However, systolic function was similar to that in control subjects. With rapid pacing, normal subjects displayed a positive contractile response, whereas this was markedly diminished in LVH subjects. With abrupt termination of pacing and return to slower sinus rhythm, LVH subjects displayed greater initial potentiation followed by a more rapid decline than control subjects, suggesting abnormalities of calcium handling. Despite contractile abnormalities, diastolic function did not further deteriorate with rapid pacing and thus did not appear to be tightly linked to the systolic changes.

CONCLUSIONS

Pacing stress in intact human LVH can result in systolic impairment superimposed on preexisting but not worsened diastolic dysfunction. Abnormal calcium handling probably contributes prominently to this response.
Use of direct angioplasty for treatment of patients with acute myocardial infarction in hospitals with and without on-site cardiac surgery. The Myocardial Infarction, Triage, and Intervention Project Investigators.
Authors: Weaver W D , Litwin P E , Martin J S
Published: June 2012

BACKGROUND

In the Myocardial Infarction, Triage, and Intervention (MITI) registry of acute myocardial infarction, 441 (12%) of 3750 patients had direct angioplasty as initial treatment. Approximately half (233) were performed in hospitals with no on-site surgery.

METHODS AND RESULTS

Procedure success rates, use of emergent surgery, and factors influencing outcome were compared in both angioplasty groups as well as with 653 patients treated with thrombolytic therapy in the same hospitals. There was no difference in baseline characteristics between patient groups treated by angioplasty in the two types of hospitals. Patency was established in 88% of patients. Only 1.4% underwent emergent surgery. Overall, survival was 93% but was significantly worse after a failed procedure in all ECG and hemodynamic subsets as well as in those with prior bypass surgery. In a multivariate analysis, age, initial heart rate, blood pressure, and prior bypass surgery but not type of hospital were predictive of survival. Survival rates were similar, but there tended to be fewer strokes (0.6% versus 2.1%, P = .12), shorter hospital stays (7.0 versus 8.1 days, P < .001), and less recurrent ischemia (20% versus 30%, P = .009) in patients treated by angioplasty compared with thrombolysis. Readmission and reinfarction rates were similar for both treatments.

CONCLUSIONS

Observations from this community registry suggest that mortality after direct angioplasty is low and the use of emergent surgery is infrequent. Outcome in this registry study was dependent on initial hemodynamic findings and infarct location but not on the presence of on-site surgery. Compared with thrombolytic therapy, the incidence of complications was the same or lower, but this needs confirmation in randomized trials.
Intracoronary albunex. Its effects on left ventricular hemodynamics, function, and coronary sinus flow in humans.
Authors: Ten Cate F J , Widimsky P , Cornel J H , Waldstein D J , Serruys P W , Waaler A
Published: June 2012

BACKGROUND

Albunex is a recently developed ultrasonic contrast agent made from sonicated human serum albumin. The effects on left ventricular hemodynamics, function, and coronary sinus flow of intracoronary Albunex in humans have not been reported.

METHODS AND RESULTS

Eighteen patients with known or suspected coronary artery disease were examined at the time of coronary arteriography with simultaneous two-dimensional echocardiography and left ventricular catheter-tip manometry. Intracoronary injections of Albunex into the left main coronary artery were performed, as were injections of 5% human serum albumin and iohexol, a widely used angiographic contrast agent. Mean coronary sinus flow was determined before and after injections of iohexol and 2 mL of Albunex. Injection of 1 mL of Albunex induced no changes in any of the measured hemodynamic parameters (heart rate, peak left ventricular [LV] systolic pressure, LV end-diastolic pressure, positive or negative LV dP/dt, or time constant of relaxation) or echocardiographic determinants of LV function (regional wall motion and global ejection fraction). Injection of 2 mL or more of Albunex caused small, transient (less than 30 seconds) changes in measures of isovolumic relaxation (negative LV dP/dt; 95% confidence interval: mean, -2.41 [-4.3, -0.52] and tau 1; confidence interval mean, 3.52; [1.48, 5.58]) but not in functional measures. Intracoronary injection of 5% human serum albumin had no effect. Iohexol induced small but significant changes in both systolic and diastolic parameters, which lasted beyond 30 seconds after injection. Mean coronary sinus blood flow increased.

CONCLUSIONS

The effects of Albunex on hemodynamics, left ventricular function, and coronary sinus blood flow compare favorably with iohexol. Albunex can be considered to be an essentially inert contrast agent if used in patients with stable coronary artery disease.
Use of inhaled nitric oxide and acetylcholine in the evaluation of pulmonary hypertension and endothelial function after cardiopulmonary bypass.
Authors: Wessel D L , Adatia I , Giglia T M , Thompson J E , Kulik T J
Published: June 2012

BACKGROUND

Increased pulmonary vascular resistance is common in congenital heart disease and is exacerbated by cardiopulmonary bypass (CPB). We investigated whether CPB is responsible for pulmonary endothelial dysfunction and contributes to postoperative pulmonary hypertension.

METHODS AND RESULTS

We infused the endothelium-dependent vasodilator acetylcholine (ACH) into the pulmonary circulation of pulmonary hypertensive children with congenital heart disease either before (n = 12) or after (n = 22) surgical repair on CPB. The dose response to ACH (10(-9) to 10(-6) M) was recorded for all hemodynamic variables. Nine additional postoperative patients were studied with ACH followed by inhalation of 80 ppm nitric oxide, an endothelium-independent smooth muscle relaxant. Plasma levels of cyclic GMP (cGMP) were measured before and after ACH and nitric oxide administration. Pulmonary vasodilation with 10(-6) M ACH was seen in all preoperative patients but was markedly attenuated in postoperative patients. Baseline pulmonary vascular resistance (5.6 +/- 1.0 U x m2) fell 46 +/- 5% in preoperative patients but declined only 11 +/- 4% from baseline (5.8 +/- 0.9 U x m2) in postoperative patients (P < .002). However, inhalation of 80 ppm nitric oxide after ACH infusion in postoperative patients lowered pulmonary vascular resistance by 33 +/- 4% (P < .0002 compared with postoperative ACH response) with minimal effects on the systemic circulation. This finding suggests that the capacity for smooth muscle relaxation and pulmonary vasodilation was present in postoperative patients but could not be induced by ACH. Plasma levels of cGMP in postoperative patients were unchanged after acetylcholine infusion but rose more than threefold during pulmonary vasodilation with nitric oxide (P < .0001). This finding is consistent with the purported role of cGMP as the second messenger effecting smooth muscle relaxation in this process.

CONCLUSIONS

CPB may be responsible for postoperative dysfunction of the pulmonary endothelial cell and may contribute to postoperative pulmonary hypertension in children. Inhaled nitric oxide is a potent pulmonary vasodilator after CPB with minimal systemic circulatory effects. It may have important diagnostic and therapeutic applications in patients with congenital heart disease.
Relation of plasma levels and composition of apolipoprotein B-containing lipoproteins to angiographically defined coronary artery disease in young patients with myocardial infarction.
Authors: Tornvall P , Båvenholm P , Landou C , de Faire U , Hamsten A
Published: June 2012

BACKGROUND

Hypertriglyceridemia is a common metabolic disturbance in men < 45 years old with myocardial infarction. To further investigate the relation between triglyceride-rich lipoproteins and severity of coronary atherosclerosis in this subset of postinfarction patients, apolipoprotein B-containing lipoproteins of 64 consecutive patients were subfractionated in connection with coronary angiography.

METHODS AND RESULTS

Density-gradient ultracentrifugation of plasma and coronary angiography were performed 4 to 6 months after the myocardial infarction. Global coronary atherosclerosis and the number and severity of distinct stenoses were evaluated by semiquantitative analysis of 15 proximal coronary segments. The majority of the patients (60%) were hypertriglyceridemic and had higher coronary scores than normotriglyceridemic patients. Of the major plasma lipoproteins, triglycerides and cholesterol in the low-density lipoprotein (LDL) fraction were associated with global coronary atherosclerosis, whereas LDL triglycerides and high-density lipoprotein (HDL) cholesterol correlated directly and inversely, respectively, with the coronary stenosis score. Plasma apolipoprotein B correlated with both coronary scores. The plasma concentrations of lipid and protein in the very-low-density lipoprotein (VLDL) subfractions (VLDL1 through VLDL3) and intermediate-density lipoprotein (IDL) did not correlate with either of the coronary scores, whereas the concentration of triglycerides in dense LDL (density > 1.040 kg/L) was strongly associated with both coronary scores. Compositional analysis of the smallest VLDL particles (VLDL3) and IDL revealed a correlation between the number of cholesteryl ester molecules in small VLDL and global coronary atherosclerosis in hypertriglyceridemic patients.

CONCLUSIONS

Global coronary atherosclerosis and distinct stenoses in young postinfarction patients are associated with the number of apolipoprotein B-containing particles in plasma and the concentration of LDL triglyceride. Specifically, dense triglyceride-rich LDL particles and, in hypertriglyceridemic patients, small cholesteryl ester-rich VLDL particles relate to coronary artery disease severity.
Transition from compensated hypertrophy to intrinsic myocardial dysfunction during development of left ventricular pressure-overload hypertrophy in conscious sheep. Systolic dysfunction precedes diastolic dysfunction.
Authors: Aoyagi T , Fujii A M , Flanagan M F , Arnold L W , Brathwaite K W , Colan S D , Mirsky I
Published: June 2012

BACKGROUND

Patients with aortic stenosis have a period of compensated left ventricular hypertrophy but may eventually develop congestive heart failure. Previous experimental studies showed either normal myocardial contractility in mild short-term pressure overload or myocardial dysfunction with severe pressure overload. Transition from compensated left ventricular hypertrophy to myocardial dysfunction has not been experimentally demonstrated in an adult large animal. Controversial issues in pressure-overload hypertrophy include whether the left ventricular dysfunction is due to insufficient hypertrophy (afterload mismatch) or to intrinsic myocardial dysfunction and whether diastolic dysfunction precedes systolic dysfunction.

METHODS AND RESULTS

We induced left ventricular hypertrophy (41% increase in left ventricular to body weight ratio) by gradually tightening a hydraulic constrictor around the ascending aorta in 9 chronically instrumented conscious sheep. Afterload (end-systolic stress) elevation remained constant (approximately 33% greater than baseline) by adjustment of the aortic constrictor over 6 weeks, gradually increasing left ventricular pressure (from 117 +/- 6 to 163 +/- 5 mm Hg) as hypertrophy developed. Four sets (baseline, 2 weeks, 4 weeks, and 6 weeks) of serial hemodynamic studies were performed in each animal with beta-blockade, first with and then without aortic constriction to mechanically match loading conditions. Stepwise methoxamine infusion was performed to obtain load-independent assessment of myocardial contractility. Midwall shortening (P < .05) and shortening rate (P < .05) at mechanically matched loading conditions showed that myocardial dysfunction developed between the fourth and the sixth week. Shortening-preload-afterload (P < .05) and shortening rate-preload-afterload (P < .05) relations, load-independent contractility indices based on the systolic myocardial stiffness concept, also revealed depressed myocardial contractility at the sixth week. Time constant of left ventricular isovolumic relaxation and diastolic myocardial stiffness constant did not change over the 6 weeks.

CONCLUSIONS

Transition from normal myocardial contractility to myocardial dysfunction was demonstrated. This transition occurred even when the elevation of afterload remained constant as hypertrophy incompletely adapted to increasing left ventricular pressure. Systolic dysfunction preceded diastolic dysfunction in this model.
Heterogeneous transmural distribution of beta-adrenergic receptor subtypes in failing human hearts.
Authors: Beau S L , Tolley T K , Saffitz J E
Published: June 2012

BACKGROUND

Downregulation of myocardial beta-adrenergic receptor density does not occur in a spatially uniform distribution in patients with congestive heart failure. Rather, it results primarily from loss of receptors in the subendocardium. In patients with dilated cardiomyopathy, beta 1-receptors have been found to be downregulated selectively. These observations suggest that considerable transmural heterogeneity in the distribution of beta-adrenergic receptor subtypes exists in the failing human heart. The present study was designed to test this hypothesis.

METHODS AND RESULTS

We used quantitative autoradiography of radioligand binding sites to measure the distribution of beta-adrenergic receptor subtypes in transmural sections of left ventricular myocardium obtained from cardiac transplant patients with ischemic (n = 13) and idiopathic dilated (n = 12) cardiomyopathy and from 4 subjects with no history of cognitive heart failure. Analysis of radioligand binding isotherms revealed a significant reduction in total beta-adrenergic receptor density in hearts of patients with ischemic and idiopathic cardiomyopathy (20.3 +/- 1.9 and 18.2 +/- 2.0 fmol/mg protein, respectively, versus 40.0 +/- 11.4 in control subjects; P < .01 for both). Loss of the beta 1-subtype accounted for 86% of the total reduction in beta-receptor density in failing hearts. Despite the significant decreases in overall tissue receptor content, the densities of total beta-receptors and beta-receptor subtypes in subepicardial myocytes were equivalent in failing and control hearts. However, in contrast to control hearts, in which the transmural distribution of total and beta 1-receptors was uniform (endocardial: epicardial receptor density ratios, 0.97 +/- 0.14 and 1.0 +/- 0.2, respectively), hearts of patients with ischemic and idiopathic dilated cardiomyopathy had significantly lower total beta-receptor and beta 1-receptor densities in the subendocardium (ratios, 0.66 +/- 0.06 and 0.46 +/- 0.09 for total and beta 1-receptors, respectively, in ischemic cardiomyopathy and 0.60 +/- 0.08 and 0.52 +/- 0.11 in dilated cardiomyopathy; P < .001 for all values compared with a ratio of 1). Thus, beta 1: beta 2 receptor density ratios were markedly decreased in the subendocardium of ischemic and idiopathic dilated left ventricles compared with control hearts.

CONCLUSIONS

A significant transmural gradient in the density of myocardial beta 1-adrenergic receptors exists in the hearts of patients with ischemic and dilated cardiomyopathy, resulting in a markedly altered beta 1: beta 2 receptor density ratio in the subendocardium.
Prognosis after the onset of coronary heart disease. An investigation of differences in outcome between the sexes according to initial coronary disease presentation.
Authors: Murabito J M , Evans J C , Larson M G , Levy D
Published: June 2012

BACKGROUND

Differences exist between men and women in prognosis after the onset of coronary heart disease (CHD).

METHODS AND RESULTS

All Framingham Heart Study subjects with the onset of clinically apparent coronary disease from 1951 through 1986 were studied to compare prognosis in men and women according to CHD presentation. Coronary disease presentations included angina, coronary insufficiency (unstable angina), recognized myocardial infarction, unrecognized myocardial infarction, and coronary death. Less than 1% of subjects were lost to follow-up for overall mortality. Cox modeling was used to examine the sex differences in outcome for each coronary presentation. New nonfatal coronary disease developed in 750 men (mean age, 63 years) and 583 women (mean age, 67 years). After onset of angina, men were at greater risk than women for myocardial infarction (hazards ratio [HR], 2.20; 95% confidence interval [CI], 1.45 to 3.34) and coronary death (HR, 2.11; 95% CI, 1.32 to 3.36) after adjustment for age and coronary disease risk factors. After a recognized myocardial infarction, there was a trend toward greater risk for overall mortality in women than men after adjustment for age and risk factors (HR, 0.75; 95% CI, 0.53 to 1.08). In contrast, after an unrecognized myocardial infarction, men were at increased risk for death compared with women (HR, 2.01; 95% CI, 1.28 to 3.15).

CONCLUSIONS

Women fare at least as poorly as men after recognized myocardial infarction, whereas women have a more favorable outlook than men after the onset of angina or unrecognized myocardial infarction. The favorable outcome in women after angina and unrecognized myocardial infarction is due, in part, to greater misclassification of these coronary events in women than in men.
Characterization of spatial patterns of flow within the reperfused myocardium by myocardial contrast echocardiography. Implications in determining extent of myocardial salvage.
Authors: Villanueva F S , Glasheen W P , Sklenar J , Kaul S
Published: June 2012

BACKGROUND

Since myocardial blood flow changes dynamically after reperfusion and since both hyperemia and impairment in microvascular function exist within the acutely reperfused bed, we sought to investigate the role of myocardial contrast echocardiography (MCE) in (1) defining the temporal variability in perfusion patterns after reflow and relating these to microsphere-derived blood flow; (2) differentiating viable from infarcted tissue during different periods of reflow; and (3) defining spatial perfusion patterns within the infarct bed in response to exogenously induced maximal vasodilation and relating these to infarct size and extent of myocardial salvage.

METHODS AND RESULTS

Twenty-one dogs with 3 hours of left anterior descending coronary artery occlusion and 2 to 3 hours of reflow were studied. MCE was performed at 15 and 45 minutes and 2 and 3 hours after reflow. It was also performed at either 2 or 3 hours after reflow in the presence of 0.56 mg/kg of dipyridamole. Radiolabeled microsphere-derived blood flow was measured at 15 minutes and 2 and 3 hours after reflow and during dipyridamole effect. Infarct size was measured at the end of the experiment by use of triphenyl tetrazolium chloride. MCE data were processed with color-coding schemes that highlighted differences in myocardial videointensities in proportion to the concentration of microbubbles within the microvasculature. There was significant variability in MCE-defined perfusion patterns after reflow, with contrast defects noted mainly within the endocardium. There were fair and significant (P < .05) correlation (r = -.73 to r = -.55) between MCE defect size and normalized endocardial blood flow. Except at 15 minutes after reflow, there was poor correlation (r = .31 to r = .51) between MCE defect and infarct sizes. Even at 15 minutes after reflow, MCE defect size underestimated infarct size by 50%. In comparison, in the presence of dipyridamole, MCE defect size correlated strongly (r = .87, P < .001) with infarct size and reasonably well with normalized transmural blood flow (r = -.62, P = .04). Moreover, the topography of the MCE perfusion defect reflected the topography of the infarct.

CONCLUSIONS

MCE revealed striking temporal heterogeneity in the spatial distribution of myocardial perfusion during postischemia reflow and either significantly underestimated or did not correlate with infarct size during reperfusion. Because of abnormalities in coronary vascular reserve specific to infarcted tissue, MCE in conjunction with intravenous dipyridamole depicted, in vivo, the actual topography of the infarct with remarkable accuracy.
Ventricular fusion during resetting and entrainment of orthodromic supraventricular tachycardia involving septal accessory pathways. Implications for the differential diagnosis with atrioventricular nodal reentry.
Authors: Ormaetxe J M , Almendral J , Arenal A , Martínez-Alday J D , Pastor A , Villacastín J P , Delcán J L
Published: June 2012

BACKGROUND

Ventricular fusion during transient entrainment of orthodromic atrioventricular reciprocating tachycardias (OAVRT) was originally found to be absent and recently observed only with left ventricular stimulation. However, previous studies were restricted to cases with a left free wall accessory pathway. The hypothesis of the present study was that fusion is likely during resetting and entrainment of OAVRT with right ventricular stimulation if the accessory pathway is septally located, since its insertion is relatively close to the stimulation site. This phenomenon can help in the differential diagnosis with atrioventricular nodal reentry (AVNR).

METHODS AND RESULTS

We performed programmed right ventricular stimulation during regular inducible supraventricular tachycardia with concentric atrial activation in 44 patients--20 with OAVRT and 24 with AVNR. Fusion in the ECG morphology of extrastimuli producing resetting was observed in 19 of 19 OAVRT but in 0 of 11 AVNR reset (P < .001). Transient entrainment was demonstrated in all 31 cases undergoing rapid ventricular pacing (14 OAVRT and 17 AVNR). Entrainment with fusion occurred in 13 of 14 OAVRT and in 0 of 17 AVNR (P < .001). Fusion was critically dependent on the coupling intervals or pacing rates, sometimes having a narrow window for its observation.

CONCLUSIONS

The relative proximity (conduction time) among pacing site, site of entrance to a reentrant circuit, and site of exit from the circuit to the paced chamber are critical for the occurrence of fusion during resetting and/or entrainment. The presence or absence of fusion during these phenomena can help in the differential diagnosis of certain supraventricular tachycardias.
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.