bluuebunny/crossref_metadata_2025 huggingface dataset:
Differing circadian patterns of symptom onset in subgroups of patients with acute myocardial infarction.
Authors: Hjalmarson A , Gilpin E A , Nicod P , Dittrich H , Henning H , Engler R , Blacky A R , Smith S C , Ricou F , Ross J
Published: June 2011

Circadian variation of the onset of acute myocardial infarction has been noted in many studies and may carry important pathophysiologic implications. However, only a few previous studies have attempted subgroup analyses. In 4,796 patients with documented acute myocardial infarction, the time of symptom onset was recorded. As in other studies, the peak of onset occurred in the morning from 6:01 AM to 12:00 noon, and 28% of the population (1.16 times the average percentage for the other time periods) experienced symptom onset in that period (p less than 0.001). There was a second, lower peak (25%) in the evening between 6:01 PM and 12:00 midnight, which was also observed in some previous studies. We sought to determine whether or not the presence of subgroups with specific clinical characteristics would exhibit different patterns and thereby contribute to these peaks in the overall population. In patients with a history of congestive heart failure (n = 606) or with non-Q wave infarction (n = 832), a pronounced peak (29%) occurred only in the evening. Two nearly equal peaks were observed in patients older than 70 years of age (n = 1,422), smokers (n = 2,057), diabetics (n = 767), women (n = 1,213), and patients taking beta-blocking drugs (n = 847). Finally, in patients with a previous myocardial infarction (n = 1,104), no peaks were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Edema of cardiac origin. Studies of body water and sodium, renal function, hemodynamic indexes, and plasma hormones in untreated congestive cardiac failure.
Authors: Anand I S , Ferrari R , Kalra G S , Wahi P L , Poole-Wilson P A , Harris P C
Published: June 2011

This study provides data on plasma hormone levels in patients with severe clinical congestive cardiac failure who had never received therapy and in whom the presence of an accumulation of excess water and sodium had been established. Eight patients were studied; two had ischemic cardiac disease, and six had dilated cardiomyopathy. Mean hemodynamic measurements at rest were as follows: cardiac index, 1.8 l/min/m2; pulmonary wedge pressure, 30 mm Hg; right atrial pressure, 15 mm Hg. Total body water content was 16% above control, extracellular liquid was 33% above control, plasma volume was 34% above control, total exchangeable sodium was 37% above control, renal plasma flow was 29% of control, and glomerular filtration rate was 65% of control. Plasma norepinephrine was consistently increased (on average 6.3 times control), whereas adrenaline was unaffected. Although plasma renin activity and aldosterone varied widely, they were on average above normal (renin 9.5 times control, aldosterone 6.4 times control). Plasma atrial natriuretic peptide (14.3 times control) and growth hormone (11.5 times control) were consistently increased. Cortisol was also increased on average (1.7 times control). Vasopressin was increased only in one patient.
Twenty-four-hour ambulatory blood pressure in shift workers.
Authors: Chau N P , Mallion J M , de Gaudemaris R , Ruche E , Siche J P , Pelen O , Mathern G
Published: June 2011

Blood pressure and heart rate of 15 male shift workers were measured every 15 minutes for 24 hours during three work shifts: morning, 4:00 AM to noon; afternoon, noon to 8:00 PM; and night, 8:00 PM to 4:00 AM. For each shift, 24-hour systolic and diastolic blood pressure showed a large "trough" (the low pressure span) and a continuous range of elevated pressure (the high pressure span). Fourier series were used to model the 24-hour blood pressure profiles. A careful examination of the residuals (measured minus predicted pressures) showed that four harmonics were necessary to describe the data accurately. The model enabled localization in each blood pressure profile of the high and low pressure spans that did not coincide with the subject's work and rest periods. The time and slope of blood pressure entering and leaving these spans could also be individually determined. Mean blood pressure during the high pressure span was the same for the three shifts, but mean blood pressure during the low pressure span was lower when the subject worked in the afternoon. During that shift, the systolic blood pressure slopes entering and leaving the low pressure span were steeper than during the two other shifts. The high pressure span was longest during the night shift and shortest during the afternoon shift. Therefore, a change in the working time profoundly perturbed the 24-hour blood pressure profile.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis impairs flow-mediated dilation of coronary arteries in humans.
Authors: Cox D A , Vita J A , Treasure C B , Fish R D , Alexander R W , Ganz P , Selwyn A P
Published: June 2011

Studies in animals have suggested that increases in blood flow result in dilation of large arteries by an endothelium-dependent mechanism. Atherosclerosis can impair endothelium-dependent vasodilation to vasoactive agents. The purpose of this study was to determine whether or not large coronary arteries in humans exhibit dilation with increases in blood flow and to test the hypothesis that this response is impaired in the presence of atherosclerosis. Graded concentrations of adenosine were infused into the distal left anterior descending (LAD) coronary artery to test the dilator response of the proximal LAD to increases in blood flow. The proximal LAD was thereby exposed to changes in blood flow, but not directly to adenosine. Ten patients with angiographically smooth proximal LAD segments (group 1) and seven patients with irregularities in the proximal LAD consistent with mild atherosclerosis (group 2) were studied. Infusions of adenosine throughout the range of 0.022 to 2.2 mg/min into the LAD produced a dose-dependent increase in estimated coronary blood flow and a mean increase of 305 +/- 27% at 2.2 mg/min adenosine. At 2.2 mg/min adenosine, a striking difference (p less than 0.001) occurred between the significant flow-mediated dilation of the proximal LAD observed in group 1 (+13.2 +/- 1.3% from 2.63 +/- 0.16 mm, p less than 0.001), and the lack of dilation in group 2 (+1.8 +/- 1.5% from 3.20 +/- 0.17 mm, p = NS), despite a greater increase in coronary blood flow in group 2 (+387 +/- 29%) than in group 1 (+230 +/- 36%).(ABSTRACT TRUNCATED AT 250 WORDS)
Flow-dependent coronary artery dilatation in humans.
Authors: Drexler H , Zeiher A M , Wollschläger H , Meinertz T , Just H , Bonzel T
Published: June 2011

To determine the role of endothelium-mediated flow-dependent coronary dilatation in humans, we studied the coronary dilatation exerted by maximal pharmacologic increase of coronary flow in 14 patients with normal coronary arteries. Biplane views of the circumflex (Cx) and left anterior descending (LAD) coronary arteries were obtained before and 80 seconds after inducing a maximal increase in flow selectively in the Cx by injecting 7 mg papaverine through a 2F infusion catheter in the midportion of the Cx (n = 10). The diameter of the proximal Cx segment (exposed to increased flow but not to papaverine directly) increased with papaverine by 11.1 +/- 4% (range, 5.2-16.4%, p less than 0.001 vs. control), whereas the LAD diameter did not change. LAD and Cx diameters increased by 18.3% and 21.2% after nitroglycerin given into the left main artery, which showed the preserved capability of the LAD to dilate. In four patients with normal coronary arteries and six patients with coronary artery disease (CAD, non-flow-limiting stenosis), a similar protocol was applied with the LAD for the assessment of flow-dependent dilatation. Simultaneously, intracoronary blood flow velocity was measured by an intracoronary Doppler catheter. Papaverine-induced coronary flow reserve (peak/resting velocity ratio) in the LAD was 4 +/- 0.7 (range, 3.5-5) in normal arteries and was 3.5 +/- 0.6 (range, 2.7-4.4) in CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
Ultrasonic tissue characterization with integrated backscatter. Acute myocardial ischemia, reperfusion, and stunned myocardium in patients.
Authors: Milunski M R , Mohr G A , Pérez J E , Vered Z , Wear K A , Gessler C J , Sobel B E , Miller J G , Wickline S A
Published: June 2011

We have previously shown in studies of experimental animals that myocardium exhibits a cardiac cycle-dependent variation of integrated backscatter that reflects regional myocardial contractile performance and that is blunted promptly after arterial occlusion and recovers after reperfusion. To define the clinical utility of ultrasonic tissue characterization with integrated backscatter for detection of acute myocardial infarction and reperfusion, 21 patients (14 men and seven women) were studied in the cardiac care unit within the first 24 hours (mean time, 11.3 hours; range, 3.5-23.8 hours) after the onset of symptoms indicative of acute myocardial infarction with conventional two-dimensional and M-mode echocardiography and with analysis of integrated backscatter. The magnitude of cyclic variation of integrated backscatter was measured from several sites within acute infarct regions and normal regions remote from the infarct zone for each patient. The average magnitude of cyclic variation among all patients (n = 21) was 4.8 +/- 0.5 dB in normal regions compared with 0.8 +/- 0.3 dB in infarct regions (p less than 0.05) within the first 24 hours after the onset of symptoms. Among the patients who had two studies, 15 (mean, 7.1 days; range, 2-31 days for second study) underwent coronary arteriography to define vessel patency. In patients with vessels with documented patency (n = 10), the magnitude of cyclic variation in infarct regions increased over time from 1.3 +/- 0.6 to 2.5 +/- 0.5 dB from the initial to final study (p less than 0.05). Patients with occluded infarct-related arteries (n = 5) exhibited no significant recovery of cyclic variation (0.3 +/- 0.3-0.6 +/- 0.3 dB). A blinded analysis of standard two-dimensional echocardiographic images revealed no significant recovery of wall thickening in either group over the same time intervals. Ultrasonic tissue characterization promptly detects acute myocardial infarction and may delineate potential beneficial effects of coronary artery reperfusion manifest by restoration of cyclic variation of integrated backscatter in the presence of severe wall motion abnormalities.
Continuous wave Doppler echocardiographic measurement of prosthetic valve gradients. A simultaneous Doppler-catheter correlative study.
Authors: Burstow D J , Nishimura R A , Bailey K R , Reeder G S , Holmes D R , Seward J B , Tajik A J
Published: June 2011

Studies correlating prosthetic valve gradients determined by continuous wave Doppler echocardiography with gradients obtained by cardiac catheterization have, to date, been limited to patients with mitral and tricuspid prostheses or have compared nonsimultaneous measurements. Simultaneous Doppler and catheter pressure gradients in 36 patients (mean age, 63 +/- 13 years) with 42 prosthetic valves (20 aortic, 20 mitral, one tricuspid, and one pulmonary) were studied. Catheter gradients were obtained using a dual-catheter technique. The simultaneous pressure tracings and Doppler flow velocity profiles were digitized at 10-msec intervals to derive the corresponding maximal and mean gradients. The correlation between the maximal Doppler gradient and the simultaneously measured maximal catheter gradient was 0.94 (SEE = 6), and that between the Doppler gradient and the simultaneously measured mean catheter gradient was 0.96 (SEE = 3). There were no significant differences in correlation between gradients for the 32 mechanical valves (maximal gradients: r = 0.95, SEE = 6; mean gradients: r = 0.96, SEE = 3) and the 10 bioprosthetic valves (maximal gradients: r = 0.89, SEE = 6; mean gradients: r = 0.93, SEE = 3). In patients with mitral prostheses, Doppler gradients correlated well with the corresponding catheter gradients obtained with direct measurement of left atrial pressure (maximal gradients: r = 0.96, SEE = 2; mean gradients: r = 0.97, SEE = 1.2). A close correlation between corresponding Doppler and catheter gradients also was found in patients with aortic prostheses (maximal gradients: r = 0.94, SEE = 6; mean gradients: r = 0.94, SEE = 3). Thus, continuous wave Doppler echocardiography can accurately predict the pressure gradient across prosthetic valves.
Magnesium content of serum, circulating mononuclear cells, skeletal muscle, and myocardium in congestive heart failure.
Authors: Ralston M A , Murnane M R , Kelley R E , Altschuld R A , Unverferth D V , Leier C V
Published: June 2011

Deranged magnesium concentrations in serum and cardiovascular structures have been implicated in the pathophysiology of hypertension, ischemic heart disease, arrhythmias, and sudden death. This study was conducted to determine the status and interrelation of serum and tissue concentrations of magnesium in patients with congestive heart failure, a clinical setting purportedly predisposed to the development of depleted levels of this cation. Magnesium concentrations of serum, circulating mononuclear cells, skeletal muscle, and myocardium were measured in 23 patients with heart failure on standard therapy. Two patients were hypomagnesemic (less than 1.6 meq/l). Poor or no correlations were found between serum and tissue magnesium concentrations and among the magnesium concentrations of the three tissues studied. Strong direct correlations were, however, noted between magnesium and potassium concentrations of the tissues examined. The prevalence of hypomagnesemia in this typical ambulatory heart failure population is relatively low (9%) and serum, circulating mononuclear cell, skeletal muscle, and myocardial magnesium concentrations correlate poorly with each other. Serum, circulating mononuclear cell, and skeletal muscle magnesium concentrations are thus of little predictive value in assessing the status of myocardial magnesium in humans with heart failure.
Detection of coronary artery stenosis in children with Kawasaki disease. Usefulness of pharmacologic stress 201Tl myocardial tomography.
Authors: Kondo C , Hiroe M , Nakanishi T , Takao A
Published: June 2011

This study determined the feasibility and accuracy of quantitative 201Tl myocardial single-photon emission computed tomography (SPECT) after dipyridamole infusion to detect coronary obstructive lesions in children with Kawasaki disease. 201Tl distribution after dipyridamole infusion was measured in 23 normal children, and with these normal values, quantitative analysis of SPECT was performed in 49 patients. Thirty-four patients had coronary stenosis 90% or greater on angiograms. Side effects resulting from systemic vasodilation were observed in about 70%. Angina pectoris and ischemic ST changes were observed only in patients with coronary stenosis. These symptoms disappeared after aminophylline infusion. Results of visual and quantitative analysis of SPECT were compared. SPECT data were shown on two-dimensional polar maps, and the extent and severity scores were calculated. The sensitivity of SPECT for detection of overall coronary stenosis was 91% (visual analysis) and 88% (quantitative analysis). The specificity of SPECT was 60% visually and 93% quantitatively. The sensitivity of quantitative analysis to detect individual coronary stenosis was similar to that of visual analysis. However, the specificity of visual analysis to detect individual coronary artery stenosis was significantly less than that of quantitative analysis. From these data, we conclude that quantitative analysis of myocardial SPECT after dipyridamole infusion is a safe and accurate diagnostic method for identifying coronary stenosis in children with Kawasaki disease.
Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation.
Authors: von Planta M , Weil M H , Gazmuri R J , Bisera J , Rackow E C
Published: June 2011

Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed venous (pulmonary artery) blood in animals and human patients during cardiac arrest and cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in 11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. Precordial compression was begun 3 minutes after onset of ventricular fibrillation and continued for 8 minutes. During CPR, there was rapid onset of profound myocardial acidosis with an increase in intramyocardial [H+] from 54 +/- 5 to 146 +/- 20 nmol/l (7.27 +/- 0.04 to 6.88 +/- 0.20 pH units). Great cardiac vein PCO2 increased from 57 +/- 2 to 158 +/- 12 mm Hg. Profound hypercarbic acidosis in great cardiac vein blood was associated with myocardial lactate production to levels of 8.1 +/- 0.7 mmol/l. Only moderate decreases in cardiac vein bicarbonate concentrations from 31 +/- 1 to 23 +/- 1 mmol/l were observed. These acid-base changes were almost completely reversed over an interval of 60 minutes after the animals were successfully resuscitated by DC countershock. The PCO2 in cardiac vein blood was significantly greater than that of mixed venous blood, demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is CO2 production during ischemia that is implicated as the predominant mechanism accounting for myocardial [H+] increases during cardiac arrest. Important clinical implications for buffer therapy during CPR and, in particular, treatment with bicarbonate emerge from these observations.
Reperfusion injury and its pharmacologic modification.
Authors: Opie L H
Published: June 2011

Reperfusion injury includes a spectrum of events, such as reperfusion arrhythmias, vascular damage and no-reflow, and myocardial functional stunning. The concept of reperfusion injury remains controversial with many proposed mechanisms when applied to humans, whereas in animal models, there are two main proposed mechanisms: calcium over-load and formation of oxygen free radicals. To prove that reperfusion injury is specifically caused by reperfusion would require evidence that an intervention given at the time of reperfusion can diminish or abolish the injury as in the case of arrhythmias, which are thought to be mediated by excess recycling of cytosolic calcium with delayed afterdepolarizations and ventricular automaticity. In the case of myocardial stunning, the phenomenon may be mediated, at least in part, by a burst of free radicals formed within the first minute of reperfusion and improved by free radical scavengers given at the time of reperfusion. The alternate hypothesis is that cytosolic calcium overload damages mechanisms for normal intracellular calcium regulation so that the stunned myocardium responds to agents that are thought to increase intracellular cytosolic calcium, such as beta-receptor agonists. A further component of reperfusion injury, under active investigation, is microvascular damage with alterations at the level of platelets, leukocytes, and endothelial integrity. From the therapeutic point of view, the divergent results of experimental interventions and the possibility that the abrupt onset of reperfusion in animals differs from the situation in humans with thrombolysis means that the best way currently available to limit reperfusion injury is by minimizing the ischemic period by early reperfusion and by optimizing the metabolic status of the ischemic myocardium at the end of the ischemic period.
Relation between central and peripheral hemodynamics during exercise in patients with chronic heart failure. Muscle blood flow is reduced with maintenance of arterial perfusion pressure.
Authors: Sullivan M J , Knight J D , Higginbotham M B , Cobb F R
Published: June 2011

We studied the central hemodynamic, leg blood flow, and metabolic responses to maximal upright bicycle exercise in 30 patients with chronic heart failure attributable to severe left ventricular dysfunction (ejection fraction, 24 +/- 8%) and in 12 normal subjects. At peak exercise, patients demonstrated reduced oxygen consumption (15.1 +/- 4.8 vs. 32.1 +/- 9.9 ml/kg/min, p less than 0.001), cardiac output (8.7 +/- 3.2 vs. 18.6 +/- 4.4 l/min, p less than 0.001), and mean systemic arterial blood pressure (116 +/- 15 vs. 135 +/- 13 mm Hg, p less than 0.01) compared with normal subjects. Leg blood flow was decreased in patients versus normal subjects at rest and matched submaximal work rates and maximal exercise (2.1 +/- 1.9 vs. 6.4 +/- 1.4 l/min, all p less than 0.01). Mean systemic arterial blood pressure was no different in the two groups at rest or at matched submaximal work rates, whereas leg vascular resistance was higher in patients compared with normal subjects at rest, submaximal, and maximal exercise (all p less than 0.01). Although nonleg blood flow was decreased at rest in patients, it did not decrease significantly during exercise in either group. Peak exercise leg blood flow was related to peak exercise cardiac output in patients (r = 0.66, p less than 0.01) and normal subjects (r = 0.67, p less than 0.01). In patients, leg vascular resistance was not related to mean arterial blood pressure, pulmonary capillary wedge pressure, arterial catecholamines, arterial lactate, or femoral venous pH at rest or during exercise. Compared with normal subjects during submaximal exercise, patients demonstrated increased leg oxygen extraction and lactate production accompanied by decreased leg oxygen consumption. Thus, in patients with chronic heart failure compared with normal subjects, skeletal muscle perfusion is decreased at rest and during submaximal and maximal exercise, and local vascular resistance is increased. Our data indicate that nonleg blood flow and arterial blood pressure were preferentially maintained during exercise at the expense of leg hypoperfusion in our patients. This was associated with decreased leg oxygen utilization and increased leg oxygen extraction when compared to normal subjects, providing further evidence that reduced perfusion of skeletal muscle is important in causing early anaerobic skeletal muscle metabolism during exercise in subjects with this disorder.(ABSTRACT TRUNCATED AT 400 WORDS)
Early improvement in left ventricular diastolic function after relief of chronic right ventricular pressure overload.
Authors: Dittrich H C , Chow L C , Nicod P H
Published: June 2011

Chronic right ventricular pressure overload is associated with left ventricular diastolic dysfunction. Whether or not an abrupt reduction in pulmonary artery pressure in patients with chronic pulmonary hypertension results in early improvement of left ventricular diastolic function is unknown. To assess this, the Doppler indexes of left ventricular diastolic function and echocardiographic measures of left ventricular volume were analyzed in 22 patients (age, 41 +/- 14 years, mean +/- SD) before and within 1 week after pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension. Mean duration of cardiopulmonary symptoms was 37 months (range, 4 months to 9 years). After operation, mean pulmonary artery pressure and pulmonary vascular resistance decreased (50 +/- 13 to 29 +/- 9 mm Hg and 904 +/- 654 to 283 +/- 243 dynes.sec/cm5, respectively, both p less than 0.001), pulmonary artery wedge pressure was unchanged (11 +/- 5 to 12 +/- 5 mm Hg), and cardiac index increased (2.0 +/- 0.5 to 2.8 +/- 0.7 l/min/m2 p less than 0.001). Left ventricular end-diastolic volume and stroke volume increased significantly (58.5 +/- 18.0 to 76.6 +/- 25.0 ml and 30.3 +/- 12.3 to 41.8 +/- 12.5 ml, respectively, both p less than 0.001) after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
Coarctation of the aorta. Long-term follow-up and prediction of outcome after surgical correction.
Authors: Cohen M , Fuster V , Steele P M , Driscoll D , McGoon D C
Published: June 2011

The long-term clinical course was studied in 646 patients, who underwent isolated operative repair of coarctation of the aorta at the Mayo Clinic from 1946 to 1981. There were 17 perioperative deaths, and 58 patients were lost to follow-up. Of the 571 patients with long-term follow-up, 11% required subsequent cardiovascular surgery, and 25% developed hypertension. There were 87 late deaths. The mean age at death was 38 years (range, 0-67 years). Estimated survival analysis revealed 91% of patients alive at 10, 84% at 20, and 72% at 30 years after operative repair. The most common cause of late death was coronary artery disease in 32 patients, followed by sudden death, heart failure, cerebrovascular accidents, and ruptured aortic aneurysm. Age, sex, and postoperative systolic blood pressure were found to be independently predictive of survival. For patients less than 14 years of age at the time of initial coarctectomy, survival to 20 years was 91%, and for patients 14 years or older at the time of operation, survival was 79%. The best survivorship was observed in patients operated on at 9 years of age or less. The higher the postoperative systolic pressure, the higher the probability of death. This study has the largest population undergoing repair of coarctation of the aorta with a median follow-up of as long as 20 years. Four main points emerged. 1) Age at the time of initial repair is the most important predictor of long-term survival. Surgery should be offered to patients after age 1 year or sooner if hypertension is severe. 2) Coronary artery disease is the most common cause of late death.(ABSTRACT TRUNCATED AT 250 WORDS)
Assessment of myocardial salvage after ischemia and reperfusion using magnetic resonance imaging and spectroscopy.
Authors: Wolfe C L , Moseley M E , Wikstrom M G , Sievers R E , Wendland M F , Dupon J W , Finkbeiner W E , Lipton M J , Parmley W W , Brasch R C
Published: June 2011

To test the hypothesis that contrast-enhanced magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) can differentiate reversible from irreversible myocardial injury, these modalities were used to study ischemia and reperfusion in a rat model. The presence of ischemia and reperfusion were confirmed with radiolabeled microspheres (n = 6). Groups of animals were subjected to either 16 (n = 17), 30 (n = 14), 60 (n = 11), or 90 (n = 14) minutes of left coronary artery (LCA) occlusion and 60 minutes reperfusion. After albumin-gadolinium (Gd)-DTPA injection, contrast-enhanced, T1-weighted, spin-echo proton images were acquired at baseline and every 16 minutes during LCA occlusion and reperfusion. In separate experiments, 31phosphorus (31P) spectra were acquired at similar time points during ischemia and reperfusion. After 16 minutes occlusion, normally perfused myocardium enhanced significantly compared with ischemic myocardium on MRI (104 +/- 7.9% vs. 61 +/- 11.0%, p less than 0.05, n = 5, mean +/- SEM, % of baseline value). MRS showed reduced phosphocreatine (PCr) and adenosine triphosphate (ATP) (58.8 +/- 2.4%, p less than or equal to 0.01; 81.4 +/- 2.4, p less than or equal to 0.01, n = 12). After 16 or 30 minutes ischemia, reflow resulted in uniform MRI signal intensity of the ischemic zone compared with normal myocardium (93.5 +/- 11.3 vs. 80.9 +/- 7.0, p = NS, n = 11, % of baseline value at 30 minutes reperfusion) and PCr recovery on MRS (94.3 +/- 4.0%, p = NS, n = 20, % baseline value at 30 minutes reflow). After 60 and 90 minutes ischemia, reflow resulted in marked enhancement of reperfused compared with normal myocardium on MRI (254.0 +/- 30.0 vs. 78.3 +/- 9.2, p less than or equal to 0.01, n = 10) and no recovery of PCr on MRS (64.1 +/- 3.0, p = NS, n = 14). Triphenyltetrazolium chloride (TTC) staining revealed transmural myocardial infarction (MI) in all hearts subjected to 60 or 90 minutes ischemia and reflow, and small nontransmural MIs in only 2/11 hearts subjected to 16 or 30 minutes ischemia and reperfusion. Thus, 1) MRI with albumin-Gd-DTPA is useful for identifying myocardial ischemia by enhancing the contrast between normally perfused and ischemic myocardia; 2) MRI with albumin-Gd-DTPA is useful for identifying reperfusion after myocardial ischemia; and 3) after reperfusion, reversible can be distinguished from irreversible myocardial injury by characteristic findings on MRI and MRS.
Acute electrophysiologic effects of sodium administration in dogs treated with O-desmethyl encainide.
Authors: Bajaj A K , Woosley R L , Roden D M
Published: June 2011

Conduction slowing is the major in vivo effect of sodium channel blocking drugs. Although this action may promote arrhythmia suppression, apparently paradoxical arrhythmia aggravation does occur. The latter outcome is most frequently seen during treatment with the class IC agents such as encainide or flecainide, which are potent depressors of conduction even at usual plasma concentrations and heart rates. Anecdotal reports in patients with such drug toxicity have suggested a beneficial effect of sodium lactate or NaHCO3 administration. The purpose of this study, therefore, was to examine the changes induced by sodium loading on the electrophysiologic properties of the canine ventricle pretreated with a class IC drug. Thirty dogs received loading and maintenance infusions of O-desmethyl encainide (ODE), an encainide metabolite that as a sodium channel blocker is approximately 10 times more potent than the parent drug. Interventions were administered during the maintenance phase when stable plasma ODE concentrations of 448 +/- 68 (SEM) ng/ml were present, and QRS was prolonged from 62 +/- 1 to 89 +/- 2 msec, and HV was prolonged from 28 +/- 1 to 50 +/- 1 msec. NaHCO3 (5 meq/kg during 1 minute) shortened QRS from 92 +/- 6 to 76 +/- 3 msec and shortened HV from 44 +/- 3 to 37 +/- 3 msec within 10 minutes (both p less than 0.01). NaHCO3 also significantly prolonged endocardial monophasic action potential duration from 231 +/- 22 to 272 +/- 33 msec and decreased serum [K+] from 3.8 +/- 0.2 to 3.0 +/- 0.2 meq/l, but it did not alter plasma ODE concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
Serial angiographic assessment of coronary artery obstruction and collateral flow in acute myocardial infarction. Report from the second Mount Sinai-New York University Reperfusion Trial.
Authors: Rentrop K P , Feit F , Sherman W , Thornton J C
Published: June 2011

In the Second Mt. Sinai-New York University Reperfusion Trial, in which change of ejection fraction was the primary end point, the following secondary end points were prospectively assessed by serial coronary angiography: patency of the infarct artery both before intervention and 10-14 days later, acute and delayed recanalization rates, presence or absence of collateral flow, and complication rates of acute interventional catheterization. We assigned 393 patients randomly to groups receiving acute cardiac catheterization and a double-blind intracoronary infusion of streptokinase (SK arm), both streptokinase and nitroglycerin (SK-NTG arm), nitroglycerin alone (NTG arm), or conventional therapy without acute catheterization (control arm). Prospective stratification was based on duration of infarct pain before randomization: group A, less than 2 hours; Group B, 2-12 hours. Baseline patency rates were comparable in patients studied within 6 hours (30%, 40 of 135) and those studied later (24%, 32 of 133). This finding refutes the hypothesis that spontaneous recanalization occurs frequently after 6 hours. The acute recanalization rates of the SK arm (60%, 40 of 67) and the SK-NTG arm (63%, 29 of 62) did not differ. During streptokinase infusion, more vessels recanalized in group A (81%, 22 of 27) than in group B (56%, 57 of 102) (p less than 0.01); this was due to a significant reduction of recanalization rates from 75% (48 of 64) to 45% (26 of 62) with treatment after 6 hours (p less than 0.01). Delayed recanalization, that is, patency at end point but not postintervention, was seen in 17% (17 of 100) of total occlusions treated with streptokinase. In group A, all total occlusions treated with streptokinase recanalized either acutely (20 of 22) or delayed (two of 22), whereas in group B, 23% (18 of 78) remained obstructed. The reocclusion rate in the SK arms was 17% (11 of 65). In the NTG arm, recanalization occurred during intervention in 4% (two of 47) and delayed in 45% (21 of 47). At end-point angiography, the patency rates of the NTG arm (62%, 41 of 66) and the control arm (58%, 36 of 62) were comparable; those of the SK arms were higher (75%, 105 of 140) (p less than 0.01). Total occlusion was associated with collateral flow in 33% (66 of 199) at baseline; the prevalence of collaterals did not increase with time to angiography, which indicates that they had developed before the index event.(ABSTRACT TRUNCATED AT 400 WORDS)
Electrophysiologic abnormalities in patients with hypertrophic cardiomyopathy. A consecutive analysis in 155 patients.
Authors: Fananapazir L , Tracy C M , Leon M B , Winkler J B , Cannon R O , Bonow R O , Maron B J , Epstein S E
Published: June 2011

Electrophysiologic studies (EPS) were performed in 155 patients with hypertrophic cardiomyopathy (HCM). Indications for EPS were cardiac arrest in 22 patients, syncope in 55 patients, presyncope in 37 patients, asymptomatic ventricular tachycardia (VT) in 24 patients, palpitations in 10 patients, and a strong family history of sudden cardiac death in seven patients. Thirty-five (23%) patients had significant resting left ventricular outflow tract obstruction. Electrophysiologic abnormalities were present in 126 (81%) patients. A high prevalence of abnormal sinus-node function (66%) and His-Purkinje (HV) conduction (30%) was noted. The most commonly induced supraventricular arrhythmias were atrial reentrant tachycardia and atrial fibrillation (10% and 11% of patients, respectively). Accessory atrioventricular pathways were present in seven (5%) patients. Programmed ventricular stimulation (PVS) induced nonsustained ventricular tachycardia in 22 (14%) patients and sustained ventricular arrhythmia in 66 (43%) patients. Sustained ventricular arrhythmia was polymorphic VT in 48 (73%) patients, monomorphic VT in 16 (24%) patients, and ventricular fibrillation in two (3%) patients. Induction was with two premature stimuli in 19 (29%) patients and three premature stimuli in 47 (71%) patients. Of 17 cardiac arrest survivors with sustained ventricular arrhythmia, 16 (94%) patients required three premature stimuli for arrhythmia induction. Sustained ventricular arrhythmia was induced at a right ventricular site in 51 (77%) patients and at a left ventricular site in 15 (23%) patients. Univariate analysis showed a significant (p less than 0.05) association between inducibility of sustained ventricular arrhythmia and VT on Holter in patients with a history of cardiac arrest or syncope but not in patients with presyncope or asymptomatic patients. Multivariate logistic regression analysis revealed that the following were significantly associated with inducibility of sustained ventricular arrhythmia: clinical presentation (cardiac arrest more than syncope more than presyncope more than asymptomatic patients, p = 0.0002; chronic or inducible atrial fibrillation, p = 0.002; and male gender, p = 0.04). In contrast, there was no clinical correlate of induced nonsustained VT.(ABSTRACT TRUNCATED AT 400 WORDS)
Feasibility of tomographic 99mTc-hexakis-2-methoxy-2-methylpropyl-isonitrile imaging for the assessment of myocardial area at risk and the effect of treatment in acute myocardial infarction.
Authors: Gibbons R J , Verani M S , Behrenbeck T , Pellikka P A , O'Connor M K , Mahmarian J J , Chesebro J H , Wackers F J
Published: June 2011

99mTc-hexakis-2-methoxy-2-methylpropyl-isonitrile (Tc-Sestamibi), a new myocardial perfusion radiopharmaceutical, was injected intravenously in 11 patients within 4 hours of the onset of acute myocardial infarction before treatment with intravenous tissue-type plasminogen activator and 6-14 days later. Five patients with acute myocardial infarction who did not receive intravenous thrombolytic therapy underwent a similar injection of radiopharmaceutical. The absence of redistribution of Tc-Sestamibi permitted imaging with single-photon emission computed tomography up to 6 hours after intravenous injection to assess the distribution of myocardial perfusion at the time of administration. The region of hypoperfused myocardium on the initial images varied widely from 9% to 68% of the left ventricle and was significantly greater in anterior than in inferior infarcts (p less than 0.01). The region of hypoperfused myocardium on the final images varied widely from 0% to 63% of the left ventricle and was also greater in anterior infarcts (p less than 0.01). The final hypoperfused region correlated (r = -0.82) with the late resting ejection fraction and with the late regional wall motion score in the infarct segment for both anterior (r = -0.74) and inferior (r = -0.97) infarcts. There was a significant decrease (-13 +/- 11%, p less than 0.003) in the extent of hypoperfused myocardium between the initial and final studies in the patients who received thrombolytic therapy compared with an insignificant increase (4 +/- 6%, p greater than 0.5) in the patients who did not receive thrombolytic therapy. Tomographic imaging with Tc-Sestamibi permits determination of the amount of hypoperfused myocardium "at risk" in acute myocardial infarction. The change in myocardial perfusion determined by Tc-Sestamibi before and after therapy in acute myocardial infarction is a promising tool for assessing treatment.
Electrocardiographic quantitation of ventricular repolarization.
Authors: Merri M , Benhorin J , Alberti M , Locati E , Moss A J
Published: June 2011

Quantification of the electrocardiographic ventricular repolarization involving the T-U wave complex is usually performed with reference to the axis of the T wave and the QT interval duration. A novel quantitative approach to improve the description of ventricular repolarization was applied to the digitized electrocardiograms of 423 normal subjects. Six electrocardiographic repolarization characteristics were identified: duration, rate, area, symmetry, late phenomena, and interlead heterogeneity. A computer algorithm was designed to automatically interpret the electrocardiographic repolarization segment and measure 11 variables that quantified these repolarization characteristics. The application of redundancy-reduction techniques selected a final set of seven variables that were used in the statistical analysis. The QT interval, which was included in the initial group of variables, was replaced by the time interval between S wave offset and T wave maximum. All selected electrocardiographic variables were independent of age (r2 less than 0.11) and body surface area (r2 less than 0.03); all except the early duration variable were heart rate- and QT interval-independent (r2 less than 0.2, r2 less than 0.13, respectively; and most were uncorrelated to each other. A comparison of repolarization characteristics by gender revealed that repolarization duration was significantly more prolonged (p less than 0.0001) in women than in men. This multidimensional quantitative approach conveys a new and more complete description of the repolarization process and provides an electrocardiographic repolarization database in normal subjects as a reference standard for identifying patients with disordered repolarization.
Solitary aortic arch artery. A result of surgical ablation of cardiac neural crest and nodose placode in the avian embryo.
Authors: Rosenquist T H , Kirby M L , van Mierop L H
Published: June 2011

Cells from the cardiac neural crest are essential for the normal development of both the heart and the great vessels. If cardiac neural crest is ablated surgically from Hamburger-Hamilton stage 9 chicken embryos, they will develop anomalies of both the heart and great vessels that are similar to anomalies that occur in humans. In the absence of cardiac neural crest, another area of neural ectoderm (nodose placode) provides replacement cells that are less competent than those of the neural crest. In this study, both the cardiac neural crest and the nodose placodes have been surgically ablated. A syndrome of unusual prevalence (47%) and severity was found among the survivors of this surgery, which was characterized by a large undivided aorta that arched dorsally without right or left deviation to become the dorsal aorta. There was no other tributary to the formation of the dorsal aorta. There were no ducti arteriosi, and the pulmonary arteries were both ectopic and hypoplastic. The brachiocephalic arteries were asymmetric and hypoplastic. The association of the aorta with the anlagen of the thyroid and thymus glands, as well as with the inferior ganglion of the vagus nerve, indicated that the solitary surviving aortic arch artery is that of arch III in this syndrome. These results establish a biological limit of the plasticity of the neural ectoderm and give a probable cellular basis for a lethal congenital septal defect.
Assessment of left-to-right atrial shunting after percutaneous mitral valvuloplasty by transesophageal color Doppler flow-mapping.
Authors: Yoshida K , Yoshikawa J , Akasaka T , Yamaura Y , Shakudo M , Hozumi T , Fukaya T
Published: June 2011

To evaluate left-to-right shunts after percutaneous balloon mitral valvuloplasty, we studied 15 consecutive patients by using transesophageal color Doppler flow-imaging system. Transesophageal color Doppler examinations were performed five times in each patient (before valvuloplasty and 1 day, 1 week, 1 month, and 6 months after valvuloplasty). No shunt flow was observed before valvuloplasty. On 1 day after mitral valvuloplasty, transesophageal color Doppler echocardiography demonstrated left-to-right shunts in 13 (87%) of 15 patients. However, a significant oxygen step-up was present in the right heart in only one patient. The mean diameter of the interatrial septal defect detected by transesophageal two-dimensional echocardiography was 1.8 +/- 1.0 mm. The mean velocity of left-to-right shunting flow measured by high-pulse repetition frequency Doppler technique was 0.83 +/- 0.38 m/sec. One week after the procedure, left-to-right shunt flow was detected in 11 (73%) patients. One month after valvuloplasty, left-to-right shunting flow was detected in seven (47%) of 15 patients. There was a significant decrease in the diameter of an interatrial septal defect between 1 day and 1 week (p less than 0.01), between 1 week and 1 month (p less than 0.01), and between 1 month and 6 months (p less than 0.05). Six months after valvuloplasty, left-to-right shunting flow remained in three (20%) patients. By using transthoracic color Doppler echocardiography, we detected left-to-right shunting flow in two patients on 1 day after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
Reversal of proarrhythmic effects of flecainide acetate and encainide hydrochloride by propranolol.
Authors: Myerburg R J , Kessler K M , Cox M M , Huikuri H , Terracall E , Interian A , Fernandez P , Castellanos A
Published: June 2011

The use of membrane-active antiarrhythmic agents may be complicated by aggravation of existing arrhythmias or development of new drug-induced arrhythmias. Four patients, referred because of out-of-hospital cardiac arrest or symptomatic sustained ventricular tachycardia, were receiving class IC antiarrhythmic agents in an attempt to prevent inducibility of sustained ventricular tachycardia. New or worsening spontaneous arrhythmias developed while they were on flecainide acetate (n = 3) or encainide hydrochloride (n = 1) therapy. Spontaneous runs of rapid nonsustained and sustained ventricular tachycardia developed in two. Increased frequency of premature ventricular contractions and repetitive forms of ventricular ectopic activity developed in one, despite the fact that inducibility of sustained ventricular tachycardia had been prevented. Salvos and nonsustained ventricular tachycardia developed in the fourth patient. Propranolol had failed to prevent inducibility of sustained ventricular tachycardia during previous programmed stimulation studies in three of the four patients, but it reproducibly suppressed drug-induced arrhythmias that appeared only after administration of the IC agents in each patient. Suppression of the proarrhythmic effects by beta-adrenergic blockade suggests a possible interaction of these drugs with autonomic function in the genesis of the observed proarrhythmic effects. Direct pharmacologic control of proarrhythmic drug effects has not previously been reported.
Exercise treadmill testing is a poor predictor of anatomic restenosis after angioplasty for acute myocardial infarction.
Authors: Honan M B , Bengtson J R , Pryor D B , Rendall D S , Stack R S , Hinohara T , Skelton T N , Califf R M , Hlatky M A , Mark D B
Published: June 2011

This study evaluated whether an exercise treadmill test could predict restenosis in 289 patients 6 months after a successful emergency angioplasty of the infarct-related artery for acute myocardial infarction. After excluding those with interim interventions (64), medical events (36), or medical contraindications to follow-up testing (25), both a treadmill test and a cardiac catheterization were completed in 144 patients, 88% of those eligible for this assessment. Four patients with left bundle branch block or pacemaker rhythm at the time of treadmill testing were also excluded from analysis. Of six follow-up clinical and treadmill variables examined by multivariable logistic regression analysis, only exercise ST deviation was independently correlated with restenosis at follow-up (chi 2 = 5, p = 0.02). The clinical diagnosis of angina at follow-up, although marginally related to restenosis when considered by itself (p = 0.04), did not add significant information once ST deviation was known. The sensitivity of ST deviation of 0.10 mV or greater for detecting restenosis was only 24% (13 of 55 patients), and the specificity was 88% (75 of 85 patients). The sensitivity of exercise-induced ST deviation for detection of restenosis was not affected by extent or severity of wall motion abnormalities at follow-up, by the timing of thrombolytic therapy or of angioplasty, or by the presence of collateral blood flow at the time of acute angiography. A second multivariable analysis evaluating the association of the same variables with number of vessels with significant coronary disease at the 6-month catheterization found an association with both exercise ST deviation (p = 0.003) and exercise duration (p = 0.04). Angina symptoms and exercise treadmill test results in this population had limited value for predicting anatomic restenosis 6 months after emergency angioplasty for acute myocardial infarction.
Prognosis in patients with low left ventricular ejection fraction after myocardial infarction. Importance of exercise capacity.
Authors: Pilote L , Silberberg J , Lisbona R , Sniderman A
Published: June 2011

The measurement of left ventricular ejection fraction (LVEF) plays a key role in many strategies for managing patients after acute myocardial infarction. We tested the hypothesis that exercise capacity 1 month after myocardial infarction provides additional information in patients with a low LVEF and therefore assists in risk stratification. One hundred fifteen patients, with documented myocardial infarction and LVEF less than 35% by gated radionuclide scan 1 month after acute myocardial infarction, were followed up for 2 months to 7 years. Exercise capacity was estimated from a treadmill test 1 month after infarction. Using the Cox proportional hazards model, exercise capacity was a significant predictor of death or reinfarction. The relative risk of death, based on a comparison between the lowermost quintile (less than 4 METS) and uppermost quintile (greater than 7 METS), was 3.5 (95% confidence interval, 1.1-9.7); the relative risk in the fourth, third, and second quintile was 2.7, 2.1, and 1.6, respectively. In a multivariate analysis, the observed effect of a good exercise capacity was independent of LVEF. These data indicate that in patients with a low LVEF after myocardial infarction, useful prognostic information can be obtained from exercise testing.