bluuebunny/crossref_metadata_2025 huggingface dataset:
The ratio of plasma high-density lipoprotein cholesterol to total and low-density lipoprotein cholesterol: age-related changes and race and sex differences in selected North American populations. The Lipid Research Clinics Program Prevalence Study.
Authors: Green M S , Heiss G , Rifkind B M , Cooper G R , Williams O D , Tyroler H A
Published: June 2011

The distribution of the ratios of plasma high-density lipoprotein cholesterol (HDL-C) to total cholesterol (TC) and of HDL-C to low-density lipoprotein cholesterol (LDL-C) are presented for 6900 white and 495 black examinees greater than 4 years old. Measurements were obtained during the visit 2 survey of the Lipid Research Clinics (LRC) Program Prevalence Study, and correspond to a 15% random sample of 60,502 participants screened during the LRC visit 1 survey. Age-specific means, medians, and selected percentiles are given by sex and by gonadal hormone use in white women. Apparent in these cross-sectional data was a consistent age-related decline in the ratio of HDL-C to TC for white male participants, from a mean of 0.360 in the age group 5 to 9 to a mean of 0.211 in the age group 50 to 54. Thereafter the mean ratio increased slightly. In white women not using gonadal hormones the age-related decline in the ratio was only evident starting at the age group 35 to 39, from which it declines from 0.329 to 0.258 in the age group 55 to 59. White women using gonadal hormones showed very minor age-related changes in the HDL-C/TC ratio, varying around a mean of 0.300. The number of blacks examined was low and thus the racial comparisons must be interpreted with caution. For each gender, age-related trends were similar in black and white study participants. Black men, however, had a higher percentage of TC carried as HDL-C than white men in all age groups examined. Black women had a higher percentage of TC in HDL-C than white women only below age 20; in the adult age range no appreciable differences were seen. Pearson correlation coefficients between the lipid, lipoprotein, and lipoprotein ratios are presented. The ratio HDL-C/TC correlated highly with the ratio HDL-C/LDL-C (greater than 0.92 for all groups) and the former may be a more conveniently determined surrogate for the latter. Although not exhaustive regarding the information it conveys about a lipid pattern, the ratio HDL-C/TC has the advantage of summarizing complex associations into a single numerical approximation.
Frequency-dependent effects of verapamil on atrioventricular nodal conduction in man.
Authors: Ellenbogen K A , German L D , O'Callaghan W G , Colavita P G , Marchese A C , Gilbert M R , Strauss H C
Published: June 2011

We sought to determine if verapamil induces frequency-dependent prolongation of atrioventricular nodal conduction in 10 consecutive patients studied in the electrophysiology laboratory. We used a maintenance infusion of verapamil designed to produce plasma concentrations of verapamil in the "therapeutic" range and that did not alter heart rate or blood pressure significantly. Frequency-dependent prolongation of atrioventricular nodal conduction (AH interval) was demonstrated in all 10 patients (p less than .001), and no change in HV conduction time with decreasing cycle length was noted in any patients while receiving verapamil. Two patterns of use-dependent response were seen. In four patients frequency-dependent prolongation of the delta(AH) interval [delta(AH) = AHverapamil - AHcontrol at a given cycle length] was seen with each decrement in pacing cycle length. In six patients frequency-dependent prolongation of the delta(AH) interval was not manifest until the fifth to eighth pacing cycle length tested. There was no association between the pattern observed and the initial heart rate or AH interval. After an abrupt change in pacing cycle length, the kinetics of delta (AH) interval prolongation were rapid; equilibrium was achieved by five to eight pulses in all patients. There was no correlation between the magnitude of prolongation of the AH interval noted at a particular cycle length and the concentration of verapamil during the maintenance infusion. These results indicate that verapamil causes use-dependent prolongation of atrioventricular nodal conduction in man.
Improvement in regional wall motion and left ventricular relaxation after administration of diltiazem in patients with coronary artery disease.
Authors: Dash H , Copenhaver G L , Ensminger S
Published: June 2011

To assess the effect of diltiazem on left ventricular systolic regional wall motion and diastolic function in patients with coronary artery disease (CAD), 22 patients underwent biplane left ventricular cineangiography before and after intravenous diltiazem (plasma concentration 154 +/- 12 ng/ml). Left ventricular and right ventricular pressures were measured by micromanometer-tipped catheters. Regional wall motion was assessed quantitatively with an area ejection fraction technique. Diltiazem decreased mean arterial pressure 11.5% (p less than .0001) and heart rate 6.8% (p less than .005); it increased cardiac index 8.8% (p less than .025) and global ejection fraction 9.1% (p less than .0001). However, left ventricular end-diastolic pressure increased 14.2% (p less than .001) and the left ventricular end-systolic pressure-volume (P-V) ratio decreased 8.8% (p less than .02). Diltiazem decreased the time constant of left ventricular relaxation by 14.3% (p less than .002), despite lack of change in the left ventricular diastolic P-V relationship, in 16 patients. Diltiazem caused a significant increase in area ejection fraction in 53% of hypokinetic areas supplied by diseased arteries compared with 13% of normokinetic areas supplied by diseased arteries (p less than .0001). Response of ejection fraction to diltiazem in areas supplied by normal coronary arteries was less (p less than .05) than that in hypokinetic areas supplied by arteries affected by disease. In conclusion, diltiazem improves regional wall motion abnormalities in patients with CAD and the improvement is associated with better left ventricular relaxation but not with a change in the diastolic P-V relationship. Global indexes of left ventricular systolic performance are favorably influenced by diltiazem, despite a mild negative inotropic effect.
Coronary thrombolysis in dogs with intravenously administered human pro-urokinase.
Authors: Collen D , Stump D , van de Werf F , Jang I K , Nobuhara M , Lijnen H R
Published: June 2011

Coronary thrombolysis was induced by infusion of highly purified human pro-urokinase isolated from a transformed kidney cell line (ACHN) or by infusion of urokinase of urinary origin in anesthetized dogs with 1-hr-old clots in the left anterior descending coronary artery. The clots were induced with a copper coil and thrombolysis was detected by repeat coronary angiography. Intravenous infusion of pro-urokinase at a rate of 10 micrograms/kg/min for 30 min in two dogs did not induce thrombolysis, which was only obtained after 8 and 15 min of its subsequent intracoronary administration. Intravenous infusion of pro-urokinase at a rate of 20 micrograms/kg/min for 30 min in four dogs induced coronary thrombolysis within 23 +/- 2 min (mean +/- SEM). This was not associated with systemic fibrinolytic activation because the alpha 2-antiplasmin and fibrinogen levels did not decrease. Intravenous infusion of urokinase at a rate of 10 micrograms/kg/min for 30 min elicited thrombolysis in four of seven dogs within an average of 19 +/- 2 min. In the other three dogs thrombolysis was only obtained within 11 +/- 3 min of its subsequent intracoronary infusion. Administration of urokinase was associated with systemic fibrinolytic activation as evidenced by a decrease of alpha 2-antiplasmin to about 10% and of fibrinogen to 43 +/- 13% of the preinfusion value. It is concluded that intravenous infusion of pro-urokinase at a sufficiently high rate produces coronary thrombolysis without systemic fibrinolysis in dogs.
Cyclic blood flow variations induced by platelet-activating factor in stenosed canine coronary arteries despite inhibition of thromboxane synthetase, serotonin receptors, and alpha-adrenergic receptors.
Authors: Apprill P , Schmitz J M , Campbell W B , Tilton G , Ashton J , Raheja S , Buja L M , Willerson J T
Published: June 2011

The phospholipid platelet-activating factor (PAF) stimulates platelet aggregation and coronary vasoconstriction. In this study we determined whether PAF alters coronary flow patterns in vivo in a canine preparation with concentric coronary artery stenosis. This preparation is characterized by cyclic flow variations in coronary blood flow associated with transient platelet aggregation at the site of the coronary constriction. Thirty-nine male mongrel dogs were used in three protocols. In protocol 1, PAF (10(-9) or 10(-8) mol/min) was infused into the coronary artery proximal to the stenosis to determine (1) whether PAF induces cyclic flow variations and (2) whether PAF has an effect on systemic hemodynamics. Cyclic flow variations were induced in three of six dogs; in these animals, mean arterial pressure decreased by 5.5% and 42.1% 10 min after infusion of the lower and higher dose of PAF. In protocol 2, cyclic flow variations were abolished with either the thromboxane synthetase inhibitor UK38485 (mean dose 2.2 mg/kg iv), the serotonin antagonist ketanserin (0.5 mg/kg iv), or the alpha 2-adrenergic antagonist yohimbine (2 mg/kg iv). Subsequent administration of PAF restored the frequency of cyclic flow variations to the preantagonist levels. Thromboxane (Tx) B2 and 6-keto-PGF1 alpha, the stable metabolites of TxA2 and prostacyclin, respectively, were measured in blood obtained distal to the coronary stenosis. TxB2 levels increased substantially during cyclic flow variations and were returned to control values with the thromboxane synthetase inhibitor UK38485. Infusion of PAF subsequently restored cyclic flow variations without altering coronary arterial coronary arterial TxB2 levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of propranolol and diltiazem alone and in combination on the recovery of left ventricular segmental function after temporary coronary occlusion and long-term reperfusion in conscious dogs.
Authors: Bush L R , Buja L M , Tilton G , Wathen M , Apprill P , Ashton J , Willerson J T
Published: June 2011

We evaluated the ability of propranolol and diltiazem alone and in combination to enhance the recovery of left ventricular (LV) segmental function during 1 month of reperfusion after two temporary occlusions of the left anterior descending coronary artery (LAD) in conscious dogs instrumented with ultrasonic crystals for the measurement of regional net systolic wall thickening (NET). LV segments were classified according to their contractile function after 1 hr of LAD occlusion: class 1, greater than 67% of preocclusion (control) NET; class 2, 0% to 66.9%; class 3, less than 0% (paradoxical systolic wall thinning). Propranolol (1 mg/kg iv) or diltiazem (20 micrograms/kg/min) was given 65 min after LAD occlusion in dogs that had 2 (group I) or 4 hr (group II) of LAD occlusion. Diltiazem plus propranolol (same doses) were given to another group of dogs that underwent 4 hr (but not 2) of LAD occlusion. Untreated control dogs received 25 ml of saline and underwent 2 or 4 hr of LAD occlusion. The NET of class 2 and 3 segments in group I control dogs increased significantly during 1 month of reperfusion, from 32 +/- 5% and -43 +/- 6% to 66 +/- 9% and 26 +/- 9%, respectively (p less than .05). Neither diltiazem nor propranolol enhanced the long-term recovery of these segments in group I dogs. However, diltiazem prevented further deterioration of contractile dysfunction observed in control dogs immediately after reperfusion in both segment classes. The NET of class 2 segments in group II control dogs after 4 weeks of reperfusion remained at levels observed during LAD occlusion: 30 +/- 4% to 37 +/- 12%. Class 3 NET increased from -33 +/- 5% to 12 +/- 12% with 1 month of reperfusion, but these segments were essentially akinetic. Propranolol or diltiazem alone did not produce significant overall increases in NET, but diltiazem again prevented further declines in NET of class 2 and 3 segments during early reperfusion. However, the combination of diltiazem and propranolol significantly enhanced overall recovery of class 2 NET in group II dogs (44 +/- 3% to 88 +/- 7%) and prevented the worsening of NET associated with early reperfusion. Compared with untreated dogs, propranolol plus diltiazem also significantly decreased the extent of histologic necrosis in class 2 and 3 segments as well as the macrohistochemically determined infarct size in group II dogs.(ABSTRACT TRUNCATED AT 400 WORDS)
Effects of unilateral stellate ganglion stimulation and ablation on electrophysiologic changes induced by acute myocardial ischemia in dogs.
Authors: Janse M J , Schwartz P J , Wilms-Schopman F , Peters R J , Durrer D
Published: June 2011

We recorded direct-current extracellular electrograms simultaneously from 60 left ventricular epicardial sites in 38 alpha-chloralose-anesthetized dogs during repeated, 5 min coronary arterial occlusions. In each dog recordings made during control occlusions were compared with those made in occlusions after, or during, the following interventions on the sympathetic nervous system: left stellate ganglion stimulation, left stellectomy, right stellectomy, and clamping the abdominal aorta with intact sympathetic nerves to induce a rise of blood pressure equal to that present during left stellate stimulation. Heart rate was kept constant. Measurements included determination of TQ segment potentials and times of local activation. After 2 min of ischemia, the degree of TQ segment depression was increased by left stellate ganglion stimulation and was decreased by both left stellectomy and clamping the aorta. Also, the area showing negative TQ potentials, indicating decreased resting membrane potentials, was enlarged by both left stellate stimulation and right stellectomy and reduced by left stellectomy. No differences were found in the results of experiments in which the left anterior descending coronary artery was occluded and those in which the circumflex branch was occluded. Left stellate stimulation significantly improved conduction within the ischemic zone. No evidence was found to suggest that the arrhythmogenic effects of left stellate stimulation and of right stellectomy, confirmed in the present study, resulted from an increased likelihood for reentry in the subepicardium of the ischemic zone.
Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts.
Authors: Gardner P I , Ursell P C , Fenoglio J J , Wit A L
Published: June 2011

The electrophysiologic and anatomic basis for fractionated electrograms were investigated in superfused epicardial preparations from infarcted canine hearts. Fractionated bipolar electrograms were frequently recorded in preparations from infarcts 2 weeks to 18 months old but only rarely in preparations from 5-day-old infarcts. The fractionated electrograms were not caused by movement artifacts. They were not associated with depressed transmembrane resting or action potentials (which were found in the 5-day-old infarcts), but rather transmembrane potentials recorded in the vicinity of the bipolar electrodes were normal. Despite the normal transmembrane potentials, activation time in regions where fractionated electrograms occurred was prolonged. However, prolonged activation time by itself did not cause fractionation, since fractionated electrograms were not recorded from normal preparations in which conduction was markedly slowed by a superfusate containing 16 mM potassium and epinephrine. Unipolar electrograms recorded with glass microelectrodes (tip size 1 to 5 microns) showed that activation in regions where fractionated electrograms were recorded was inhomogeneous. Prepotentials were found preceding the upstrokes of some action potentials in regions where double potentials were recorded, suggesting the possibility of electrotonic transmission across high resistance or inexcitable gaps, but no electrotonic potentials were seen in regions with multicomponent fractionated electrograms. Fractionated electrograms were recorded in regions where infarct healing caused wide separation of individual myocardial fibers while distorting their orientation. The anatomic changes probably caused slow and inhomogeneous activation.
Interruption of sympathetic and vagal-mediated afferent responses by transmural myocardial infarction.
Authors: Barber M J , Mueller T M , Davies B G , Gill R M , Zipes D P
Published: June 2011

We have demonstrated previously that sympathetic and vagal afferents travel in an apical-to-basal course in the heart, and can be stimulated selectively with epicardial applications of bradykinin and nicotine, respectively. In this study we tested the hypothesis that transmural myocardial infarction interrupts sympathetic and vagal afferent fibers traveling through the infarction and produces regions of afferent denervation in areas apical to the infarction. In open-chest, chloralose-anesthetized dogs, transmural myocardial infarction was created by embolizing a diagonal branch of the left anterior descending coronary artery with a vinyl latex solution that was injected directly into the artery and hardened rapidly. The transmural nature of the infarction was verified by the nitro blue tetrazolium staining technique for dehydrogenase enzymes. Epicardial applications of bradykinin (5 micrograms) and nicotine (50 micrograms) were used to stimulate chemically sensitive sympathetic and vagal afferent nerve endings, respectively. Twenty-nine dogs were studied before and 90 min after creation of transmural myocardial infarction. In 20 dogs, epicardial bradykinin applied before production of transmural myocardial infarction produced a maximal pressor response of 13 +/- 3 mm Hg 40 sec after application (p less than .01 vs preapplication values), while topical nicotine produced a maximal depressor response of 14 +/- 2 mm Hg (p less than .01 vs preapplication values) 20 sec after application at all sites tested. Ninety minutes after production of transmural myocardial infarction, epicardial sites basal to the infarction continued to respond normally to both drugs, while sites within the area of infarction and apical to the area (noninfarcted myocardium) no longer showed a pressor response to topical bradykinin or a depressor response to topical nicotine.(ABSTRACT TRUNCATED AT 250 WORDS)
Left ventricular ejection fraction after acute coronary occlusion in conscious dogs: relation to the extent and site of myocardial infarction.
Authors: Schneider R M , Chu A , Akaishi M , Weintraub W S , Morris K G , Cobb F R
Published: June 2011

The change in left ventricular radionuclide ejection fraction after acute occlusion of the left anterior descending (LAD) or circumflex (LC) coronary artery was compared with the ultimate histologic extent of myocardial infarction in conscious dogs. The acute change in ejection fraction correlated with size of infarction in 14 dogs with occlusions of the LAD coronary artery (r = .89, y = 1.12x + 14.2) and in 27 dogs with occlusions of the LC coronary artery (r = .71, y = 0.73x + 7.9); the slope of the regression equation was greater (p less than .05) for those with LAD than for those with LC occlusions. Multivariate analysis revealed no independent contribution of left ventricular weight, the subendocardial extent of infarction, or change in heart rate to the acute change in ejection fraction. These data indicate that the decrease in ejection fraction after coronary occlusion is determined primarily by the size of the ischemic area, which also determines size of infarction. In dogs instrumented over a long term, infarcts in the LAD myocardial distribution result in greater decreases in ejection fraction than infarcts of comparable size in the LC distribution.
A potential method of correcting intracavitary left ventricular filling pressures for the effects of positive end-expiratory airway pressure.
Authors: Ditchey R V , Lindenfeld J , Grogan E W , Zerbe G O
Published: June 2011

Based on the observation that positive end-expiratory airway pressure (PEEP) causes comparable increments in intrapericardial and right-sided intracardiac pressures, we hypothesized that intracavitary left ventricular filling pressures measured in the presence of PEEP can be corrected for increased intrathoracic pressure by subtracting the effects of PEEP on intracavitary right ventricular filling pressures. Ventricular function curves (aortic blood flow vs intracavitary left ventricular end-diastolic pressure [LVEDP]) were generated with and without 15 cm of water of PEEP in eight dogs. All curves were shifted to the right by PEEP (i.e., intracavitary LVEDP was higher for any submaximal level of aortic blood flow). However, when pressures measured in the presence of PEEP were "corrected" by subtracting the corresponding increment in intracavitary right ventricular end-diastolic pressure caused by PEEP at each level of ventricular filling, control and corrected PEEP data points appeared to fall on the same curve in five dogs, and differed only slightly in three dogs. Mean control and corrected PEEP curves derived by averaging polynomial regression coefficients for each condition differed significantly from uncorrected PEEP curves (p less than .05), but not from each other. Analogous curves based on mean left atrial pressure were corrected equally well by subtracting the effects of PEEP on mean right atrial pressure. We conclude that the increments in intracavitary right heart filling pressures caused by PEEP can be used to correct intracavitary left heart filling pressures for the effects of PEEP on intrathoracic pressure.
Evidence for 15-HETE synthesis by human umbilical vein endothelial cells.
Authors: Gorman R R , Oglesby T D , Bundy G L , Hopkins N K
Published: June 2011

Incubation of cultured human umbilical vein endothelial cells with [1-14C]-arachidonic acid, followed by RP-HPLC analysis, resulted in the appearance of two principal radioactive products besides 6-keto-PGF1 alpha. The first peak was HHT, a hydrolysis product of the prostaglandin endoperoxide. The second peak was esterified, converted to the trimethylsilyl ether derivative, and analyzed by GC/MS and was shown to be the lipoxygenase product 15-HETE. Stimulation of endothelial cells with thrombin enhanced 15-HETE synthesis from arachidonate. Subsequent experiments showed that 5-HETE and 12-HETE were also synthesized by endothelial cells, but no evidence of leukotriene synthesis was found. Incubation of the 15-HETE precursor 15-HPETE with endothelial cells resulted in the formation of four distinct ultraviolet light-absorbing peaks. Ultraviolet and GC/MS analysis showed these peaks to be 8,15-diHETEs that differed only in their hydroxyl configuration and cis-trans double-bond geometry. Formation of 8,15-diHETE molecules suggests the prior formation of the unstable epoxide molecule 14,15-LTA4 or an attack at C-10 of 15-HPETE by an enzyme with mechanistic features in common with a 12-lipoxygenase. The observation that endothelial cells can synthesize both 15-HETE and 8,15-diHETE molecules suggest that this cell type contains both a 15-lipoxygenase and a system that can synthesize 14,15-LTA4.
Noninvasively diagnosed peripheral arterial disease as a predictor of mortality: results from a prospective study.
Authors: Criqui M H , Coughlin S S , Fronek A
Published: June 2011

Intermittent claudication has been reported in previous studies to approximately double the risk of subsequent mortality. However, a history of claudication is often present in the absence of significant peripheral arterial disease (PAD) and absent in the presence of PAD. For this reason we evaluated the association between large-vessel and small-vessel PAD, measured by highly reliable and valid noninvasive tests, and mortality in 567 older subjects from a defined population followed-up for an average of 4 years. Large-vessel PAD was strongly and significantly predictive of all-cause mortality in both men and women with a relative risk of 4 to 5, and this finding was independent of other cardiovascular disease risk factors in multivariable analysis. In addition, this finding persisted after exclusion of subjects with extant cardiovascular disease at baseline. The associations of both claudication and abnormal peripheral pulses with mortality were weaker than the large-vessel PAD association. Isolated small-vessel PAD was unrelated to subsequent mortality. These findings suggest older subjects of both sexes at a high risk of impending mortality can be identified through noninvasive testing for large-vessel PAD.
Subendocardial infarction in retrospect: pathologic, cardiographic, and ancillary features.
Authors: Levine H D
Published: June 2011

Fifty-three patients with subendocardial infarction (SEMI) were studied at autopsy; all were elderly and the group was equally divided by sex. About half had more than one SEMI; the recurrences or extensions often involved superjacent, but not infrequently adjacent, areas. Six showed fibrinous pericarditis. This larger study showed more widespread and severe coronary narrowing than an earlier report. Six patients had thrombi in the right coronary artery. Six showed electrocardiographic evidence of concomitant anteroseptal and inferior (Roesler-Dressler) infarction, and 12 had intraventricular block generally preceding higher-grade block or arrhythmias. At some time during their terminal hospitalization, 27 patients, or half, developed distinctive protracted RS-T depression or T wave inversion. Twenty-four of the SEMIs were diagnosed on accepted criteria as transmural infarct; that diagnosis was sustained in only four. Thus neither the presence of changes in RS-T segment or T wave nor the absence of QRS changes are mandatory for the diagnosis of SEMI; this invalidates the common assumption that the diagnosis is not justified unless these conditions are met.
Autonomic control of ventricular tachycardia: sympathetic neural influence on spontaneous tachycardia 24 hours after coronary occlusion.
Authors: Martins J B
Published: June 2011

This study was performed to determine whether sympathetic nerves influence the rate of ventricular tachycardia occurring spontaneously in dogs 24 hr after occlusion of the anterior descending coronary artery. Seventeen chloralose-anesthetized dogs underwent activation mapping during spontaneous ventricular tachycardia with QRS morphologies similar to those recorded in the conscious state. Bilateral stellate ganglionectomy (n = 8) decreased mean arterial pressure from 71 +/- 4 (mean +/- SE) to 52 +/- 5 mm Hg (p less than .001) and heart rate from 121 +/- 9 to 79 +/- 15 beats/min (p less than .025) by decreasing the number of complexes of ventricular tachycardia from 120 +/- 9 to 49 +/- 15 per minute (p less than .001). Subsequent unilateral sympathetic nerve stimulation (n = 4) was shown to accelerate ventricular tachycardia foci originating from the ipsilateral aspect of the infarction. Regional sympathetic denervation (n = 7) was performed by application of phenol to the epicardium surrounding an electrode at the site of origin of at least one morphology of ventricular tachycardia. Mean arterial pressure did not change, but total heart rate decreased from 122 +/- 9 to 106 +/- 9 beats/min (p less than .01) and the number of complexes of ventricular tachycardia with a morphology arising from the phenol-treated area fell from 68 +/- 12 to 28 +/- 9 (p less than .001). Evidence for regional denervation was documented by prolongation of duration of electrograms and local repolarization times limited to the phenol-treated area. We conclude that sympathetic nerves directly control rate of spontaneous ventricular tachycardia 24 hr after myocardial infarction in the dog.
Intraoperative detection of myocardial ischemia in high-risk patients: electrocardiography versus two-dimensional transesophageal echocardiography.
Authors: Smith J S , Cahalan M K , Benefiel D J , Byrd B F , Lurz F W , Shapiro W A , Roizen M F , Bouchard A , Schiller N B
Published: June 2011

Because acute segmental wall motion abnormalities (SWMAs) of the left ventricle are highly sensitive and specific indicators of myocardial ischemia, this study compared the incidence and significance of ischemia, as detected by two-dimensional transesophageal echocardiography and surface electrocardiography, during anesthesia and surgery in patients at high risk of myocardial ischemia. During surgery, 24 of the 50 patients studied had new SWMAs, whereas only six had ST segment changes. All patients with ST segment changes also had new SWMAs: in three instances, SWMAs occurred before the ST segment change, and in three instances, they occurred simultaneously. All three patients who had intraoperative myocardial infarctions also had persistent intraoperative SWMAs, whereas only one patient had ST segment changes. Ten healthy patients requiring noncardiovascular surgery were monitored similarly; none of these had SWMAs, ST segment changes, or myocardial infarction. This study demonstrates the superiority of two-dimensional transesophageal echocardiography over electrocardiography for the intraoperative detection of myocardial ischemia. Furthermore, when new SWMAs persist to the conclusion of surgery, myocardial infarction is likely to have occurred.
Transcutaneous oxygen recovery and toe pulse reappearance time in the assessment of peripheral vascular disease.
Authors: Kram H B , White R A , Tabrisky J , Appel P L , Fleming A W , Shoemaker W C
Published: June 2011

The accuracy of measurements of transcutaneous oxygen tension (Ptco2) in the diagnosis of peripheral vascular disease (PVD) may be significantly increased by stressing limb circulation with the use of temporary ischemia. The purpose of this study was to compare the transcutaneous oxygen recovery half-time (TORT) and the toe pulse reappearance time (PRT/2) in a series of patients with symptomatic PVD before and after vascular reconstruction. The TORT was defined as the time required to recover half of the decrease in the limb/chest Ptco2 ratio caused by temporary limb ischemia, and is conceptually comparable to the toe PRT/2, the time required to recover half of the control toe pulse amplitude. Measurement of TORT was found to be more feasible (100% vs 58%) and to have a greater diagnostic yield (100% vs 92%) than that of the toe PRT/2. When measured on the dorsum of the foot, TORT values were found to correlate well with the severity of symptoms of PVD; toe PRT/2 values did not correlate with severity of symptoms. Patients who underwent successful vascular reconstruction had significant improvement in their calf and foot TORT values after surgery (p less than .005 and .0005, respectively); postoperative values were similar to those obtained in normal subjects. Toe PRT/2 values usually improved postoperatively, but in many patients postoperative values overlapped with values that were considered abnormal. There was no overlap of TORT values in normal subjects with those in patients with symptomatic PVD. The measurement of TORT may be clinically useful for screening patients with suspected PVD and for assessing quantitatively the results of conservative and surgical therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Computer detection of atrioventricular dissociation from surface electrocardiograms during wide QRS complex tachycardias.
Authors: Slocum J , Byrom E , McCarthy L , Sahakian A , Swiryn S
Published: June 2011

Differentiation of wide QRS complex tachycardias on surface electrocardiograms is difficult for physicians and computers due in part to their inability to identify atrial activity, specifically atrioventricular (AV) dissociation. We studied 20 examples of AV associated rhythms and 17 examples of AV dissociated ventricular tachycardia. We applied an algorithm consisting of subtraction of a mean beat from each individual beat in leads II and V1 to generate remainder electrocardiograms. The remainder electrocardiograms were visually inspected for the presence of P wave candidates and then autocorrelated. AV dissociated P wave candidates were evident on visual inspection of remainder electrocardiograms in none of 20 AV associated and 15 of 17 AV dissociated rhythms. Atrial cycle length and the presence of AV dissociation were automatically detected by applying a peak selection algorithm to the autocorrelation function. AV association was detected in all 20 AV associated rhythms and AV dissociation was detected for 11 of 17 AV dissociated rhythms (sensitivity 65%, specificity 100%, positive and negative predictive accuracy 100%, 77%). The correlation coefficient of detected vs true atrial cycle length for the 11 correctly detected AV dissociated rhythms was r = .98. Visual inspection of the remainder electrocardiograms along with the original electrocardiogram may increase the ease with which human readers can identify the presence of AV dissociation and thus diagnose ventricular tachycardia. Computer diagnosis of wide QRS complex tachycardias should be significantly improved by use of this algorithm.
Comparison of pathologic and angiographic findings in a porcine preparation of coronary atherosclerosis.
Authors: Weiner B H , Ockene I S , Jarmolych J , Fritz K E , Daoud A S
Published: June 2011

Coronary atherosclerosis was induced in Yorkshire swine by diet-induced hyperlipidemia and balloon intimal abrasion of a coronary artery. Severe stenoses pathologically similar to the lesions of human atherosclerosis were seen after 8 months of the atherogenic regimen. To examine the relationship between the angiogram and pathology in the assessment of the extent and location of coronary atherosclerosis, antemortem angiographic results were compared with results of pathologic examination. Vernier caliper measurements of the coronary angiogram were compared with results of morphometric evaluation of perfusion-fixed coronary arteries. Isolated focal stenoses were correctly localized and quantified, as were focal lesions within vessels diffusely diseased. Both overestimation and underestimation of lesions occurred at bifurcation sites. Diffuse disease without focal stenoses was not well demonstrated angiographically. Vessels that were angiographically thought to be normal or only minimally diseased demonstrated significantly larger lumens angiographically than pathologically. This is believed to be due to fixation and paraffin-processing artifact, even though fixation was performed by perfusion at physiologic pressure. The demonstration of an excellent correlation between the luminal size as determined angiographically and morphometrically at sites of focal obstruction confirms the value of quantitation of coronary angiograms in vivo as a diagnostic tool in coronary atherosclerosis.
Uptake of hematoporphyrin derivative by valvular vegetations in experimental infective endocarditis.
Authors: Spokojny A M , Sinclair I N , Schnitt S , Paulin S , Spears J R
Published: June 2011

Drugs that localize in valvular vegetations may be useful in the diagnosis and treatment of infective endocarditis. We therefore tested the hypothesis that parenterally injected hematoporphyrin derivative (HPD), which is concentrated in tumors and atherosclerotic plaques, localizes in the vegetations of experimental infective endocarditis. In 14 rabbits, various bacteria were given intra-arterially immediately after injury to the aortic valve. In 12 additional rabbits, sterile vegetations on the aortic valve were produced by the trauma caused by an indwelling catheter that had been in place over a long period. HPD, 2.5 mg/kg, was injected intravenously 1 to 2 days before the animals were killed in six rabbits with sterile vegetations and in seven rabbits with infected vegetations. In all rabbits, multiple vegetations on the aortic valve leaflets were identified. On exposure to ultraviolet light, strong porphyrin fluorescence of all vegetations, whether sterile or infected, was observed only in rabbits given HPD. In two rabbits given HPD 10 weeks after catheter implantation across the aortic valve, however, only mild fluorescence could be detected in healing endocardial vegetations. In frozen sections of HPD-laden lesions, a patchy distribution of fluorescence was observed that was similar to the pattern of HPD localization in atheromatous plaques. Since vegetations in experimental infective endocarditis selectively concentrate HPD, porphyrins could be useful in the diagnosis and treatment of infective endocarditis.
Contrast echocardiographic estimation of regional myocardial blood flow after acute coronary occlusion.
Authors: Kemper A J , Force T , Kloner R , Gilfoil M , Perkins L , Hale S , Alker K , Parisi A F
Published: June 2011

Contrast echocardiography can predict pathologic area at risk during acute coronary occlusion. In this study we evaluated (1) whether the intensity and timing of contrast appearance in ischemic regions can provide a quantitative measure of residual myocardial perfusion, and (2) whether changes in these parameters observed after serial injections reflect changes in blood flow to acutely ischemic tissue. Supra-aortic hydrogen peroxide contrast echocardiography was performed in 12 consecutive dogs at 1, 20, and 120 min after acute circumflex coronary occlusion. Contrast enhancement was determined qualitatively with a segmental four-point scoring system based on the appearance time and peak perceived intensity of contrast enhancement and quantitatively with a computer algorithm designed to reflect these parameters. Comparison was made in each segment to concomitant radioactive microsphere blood flow. Qualitative scoring related systematically to normalized segmental blood flow (3+ = 93%; 2+ = 61%; 1+ = 32%; 0 = 18%; p less than .01 for each vs adjacent value), as did quantitative analysis including all segments (r = .78; p less than .01) and isolated to the ischemic region (flow = 1.13 intensity change +6.8%; r = .83, p less than .001). Changes in microsphere flow in ischemic regions between sequential observations were correlated with changes in qualitative score (r = .88, p less than .001) and results of quantitative analysis (r = 0.70, p less than .01). The amount of contrast enhancement can provide quantitative information about residual myocardial blood flow in ischemic regions and can also be used to track changing patterns of flow in vivo after acute coronary occlusion.
The relationship of white cell count, platelet count, and hematocrit to cigarette smoking in adolescents: the Oslo Youth Study.
Authors: Tell G S , Grimm R H , Vellar O D , Theodorsen L
Published: June 2011

This article reports on the relationship between cigarette smoking, white blood cell count (WBC), platelet count (PC), and hematocrit in a Norwegian adolescent population. Data were obtained on 439 youths, 14 to 16 years old, as part of the Oslo Youth Study, an investigation of risk factors and behaviors for cardiovascular disease and cancer among adolescents. Analyses of covariance, controlling for height, weight, age, sexual maturation, high-density lipoprotein (HDL) cholesterol, and hematocrit revealed that both male and female regular smokers (those reporting smoking at least once a week) had significantly higher mean WBCs. Male regular smokers also had significantly higher PCs than nonsmokers, and female regular smokers had higher PCs than young women who smoked less often than once a month. Hematocrit, after adjustment for height, weight, age, sexual maturation, and HDL cholesterol, was significantly lower in male regular smokers, while female regular smokers had higher hematocrit values than nonsmokers or occasional smokers. Results of this study show that WBC and PC were increased in adolescents who started smoking relatively recently. This indicates that the increase in white cell count observed in smokers is unlikely to be due to a longstanding smoking-induced chronic disease condition.
Has 'obstruction' hindered our understanding of hypertrophic cardiomyopathy?
Authors: Criley J M , Siegel R J
Published: June 2011

HCM is a disorder associated with significant morbidity and mortality and a propensity to cause sudden, often unexpected death. The similarity to the symptom complex of aortic stenosis and the presence of a pressure gradient justified the initial assumption that obstruction was of prime importance in HCM and that relief of obstruction was the focal point of rational therapy. However, it is our belief that the dogma of obstruction has impeded progress in and obscured the understanding of HCM and interpretation of its manifestations. The purpose of this article is to call attention to significant discrepancies in the obstructive concept that have been reinforced as new techniques emerged that have allowed further study of the disease. Since neither the presence of a gradient nor SAM can be justifiably equated with the presence of an obstruction, it is proposed that the appellation "obstruction" be reserved for those cases in which the rate of outflow or the rate or degree of ventricular emptying are demonstrably impeded, as in aortic stenosis. Therapy with beta-adrenergic-receptor and calcium channel-blocking agents have shown promise for alleviating symptoms and possibly prolonging life without systematically or predictably affecting the pressure gradient, probably because of their beneficial effects on ventricular relaxation and diastolic filling. Antiarrhythmic therapy has been effective in reducing mortality. Ideally, prevention or regression of the pathologic hypertrophy should be the major focus of future therapeutic interventions in hypertrophic cardiomyopathy.
Effect of beta-adrenergic blockers on the peripheral circulation in patients with peripheral vascular disease.
Authors: Hiatt W R , Stoll S , Nies A S
Published: June 2011

Beta-Adrenergic blockers have not been widely used in patients with peripheral vascular disease because these drugs have been reported to worsen the symptoms of intermittent claudication. To test this assumption we studied the effects of a beta 1-selective and a nonselective beta-adrenergic blocker on postexercise calf blood flow and symptoms of claudication in 19 patients with mild-to-moderate peripheral vascular disease. Subjects received placebo for 3 weeks, and then were randomized to 120 mg/day propranolol or 150 mg/day metoprolol with the use of a crossover design. Blood flow in the calf was measured by strain-gauge plethysmography at rest and immediately after exercise on a bicycle ergometer at a low and a high workload. The symptoms of claudication were monitored during bicycle exercise and by patient diaries maintained between visits. Maximal exercise heart rate was reduced an equivalent amount by metoprolol (19 beats/min) and propranolol (16 beats/min). Mean arterial pressure was reduced by propranolol at rest and by both drugs with exercise. Calf blood flow was not affected by either drug compared with placebo at rest or at either workload. In addition, the symptoms of claudication were not worsened by either drug. We conclude that despite evidence of beta 1-adrenergic blockade and a lowering of arterial pressure, neither beta-adrenergic blocker adversely affected the peripheral circulation.
Significance of cardiac defects in the developing fetus: a study of spontaneous abortuses.
Authors: Ursell P C , Byrne J M , Strobino B A
Published: June 2011

We investigated the impact of heart defects on the developing human fetus by examining 412 hearts from consecutive spontaneous abortuses. In each case, the cardiac morphology was correlated with the autopsy findings and the karyotype (unavailable in 115 hearts not successfully cultured). Of the 412 hearts, 10 (2.4%) contained structural defects (six ventricular septal defects, one atrial septal defect with ventricular septal defect, and one each coarctation, atrioventricular septal defect, and tetralogy of Fallot). Only one of 10 had major extracardiac malformations. Of the 277 fetuses with normal karyotype, three (1.1%) had heart defects. Of the 20 fetuses with abnormal karyotype, four (20%) had heart defects. In the remaining three fetuses with heart defects, the karyotype was not obtained. Thus (1) 57% of spontaneous abortuses with congenital heart defects contained major chromosomal abnormalities, (2) the spectrum of heart defects among spontaneous abortuses was similar to that among liveborns, and (3) since the prevalence of heart defects among fetuses without other major abnormalities was similar to that among liveborns, heart defects alone may not jeopardize the survival of a developing fetus.
Effect of isotonic exercise training on left ventricular volume during upright exercise.
Authors: Crawford M H , Petru M A , Rabinowitz C
Published: June 2011

To determine the changes in left ventricular volume and their time course during exercise we studied 30 runners. Left ventricular end-diastolic and end-systolic volumes were measured from biapical two-dimensional echocardiograms recorded during graded upright bicycle exercise. The validity of this echocardiographic technique was assessed by comparing measurements at rest and exercise with results obtained by gated equilibrium radionuclide angiography in 10 patients with coronary artery disease. Although the absolute volume measurements were lower by echocardiography, ejection fraction was not significantly different and the directional changes in volume during exercise were comparable. In the runners, resting left ventricular end-diastolic volume measurements by echocardiography correlated with their maximum bicycle exercise endurance times (r = .80). Left ventricular end-diastolic volume, stroke volume, and ejection fraction increased during exercise with the most marked changes occurring in the first half of exercise. Systolic blood pressure/end-systolic volume (SBP/ESV) also increased during exercise, but the largest change occurred during the second half of exercise. Left ventricular volumes were larger in the 12 competitive marathon runners (maximum exercise duration greater than or equal to 27 min) as compared with the 18 noncompetitive runners (exercise duration less than or equal to 23 min): resting end-diastolic volume 130 +/- 29 (SD) ml vs 87 +/- 20 ml (p less than .001), respectively. During exercise the competitive runners exhibited a larger increase in end-diastolic volume and the noncompetitive athletes showed a greater increase in SBP/ESV. Therefore, highly trained competitive marathon runners make greater use of the less energy-consuming Frank-Starling mechanism to accomplish high levels of isotonic exercise performance as compared with less well-trained runners.