bluuebunny/crossref_metadata_2025 huggingface dataset:
Effects and mechanism of action of aminophylline on cardiac function and regional blood flow distribution in conscious dogs.
Authors: Rutherford J D , Vatner S F , Braunwald E
Published: June 2011

The effects of aminophylline, 1 mg/kg/min infused intravenously for 10 minutes, were examined on left ventricular (LV) diameter, pressure, an indexes of myocardial contractility, as well as systemic, coronary and regional hemodynamics in conscious dogs. Aminophylline increased mean arterial pressure 12 +/- 2%, LV systolic pressure 8 +/- 1%, LV dP/dt 20 +/- 2%, velocity of myocardial fiber shortening 13 +/- 2% and heart rate 5 +/- 2%, and reduced LV end-diastolic diameter 2 +/- 0.5%. Vascular resistance rose in the systemic bed 13 +/- 5%, the coronary bed 26 +/- 3%, the mesenteric bed 26 +/- 5% and the iliac bed 36 +/- 4%, but did not rise in the renal bed. Both beta-adrenergic receptor blockade with propranolol and chronic treatment with reserpine attentuated but did not abolish the positive inotropic response induced by aminophylline. Alpha-adrenergic receptor blockade with phentolamine prevented aminophylline-induced vasoconstriction in the systemic, coronary, mesenteric and iliac beds. In contrast to the vasoconstriction with i.v. aminophylline, when the drug was infused directly into the iliac artery, it elicited marked iliac vasodilation. Thus, in the intact conscious dog, i.v. aminophylline, in a dose that had little effect on heart rate, increased LV contractility and reduced preload. The increase in contractility was dependent in part on intact beta-adrenergic nervous activity and endogenous catecholamine stores. The increase in systemic, coronary, iliac and mesenteric resistances involved alpha-adrenergic mechanisms. These actions appear to involve autonomic mechanisms, because the only direct effect of aminophylline on the iliac artery was marked vasodilation.
Double-outlet right ventricle: wide-angle two-dimensional echocardiographic observations.
Authors: Hagler D J , Tajik A J , Seward J B , Mair D D , Ritter D G
Published: June 2011

M-mode echocardiographic delineation of double-outlet right ventricle (DORV) has relied primarily on the demonstration of mitral-semilunar valve discontinuity--a feature that requires an interpretation of spatial anatomic relationships. Thirty-six patients with DORV were examined by wide-angle real-time two-dimensional echocardiography. Anatomic diagnosis was established by surgery in 28 patients and by angiography alone in eight. Typical two-dimensional echocardiographic features were (1) parallel orientation and origin of both great arteries from the anterior right ventricle, (2) mitral-semilunar valve discontinuity demonstrated on parasternal long-axis scans by the presence of muscular conus separation, and (3) absence of left ventricular outflow other than a ventricular septal defect. This technique also allows better recognition of spatial orientation of the great arteries and the position of the ventricular septal defect relative to the great arteries. An unexpected finding was a high incidence of atrioventricular valvular anomalies, particularly annular override or abnormal chordal attachments (straddling) (eight patients), isolated cleft of the mitral valve (two patients), and complete atrioventricular canal (five patients). Thus, these two-dimensional echocardiographic findings have allowed improved noninvasive recognition of DORV and the demonstration of associated anomalies that previously were unrecognized preoperatively.
Endothelial cell damage and thrombus formation after partial arterial constriction: relevance to the role of coronary artery spasm in the pathogenesis of myocardial infarction.
Authors: Gertz S D , Uretsky G , Wajnberg R S , Navot N , Gotsman M S
Published: June 2011

The left anterior descending coronary artery of four dogs and the right common carotid artery of 15 rabbits were subjected to 40-60% reduction in transluminal diameter for 1 hour by partial ligation with suture thread. Scanning electron microscopic examination of the luminal surface of these vessels revealed endothelial craters and balloons, fragmentation and desquamation on the proximal slope of the constriction. Platelet attachment to exposed subendothelial tissues was clearly evident, and microthrombi were seen at the point of maximum constriction. Blood flow, as measured by electromagnetic flow probe, was virtually unchanged upon partial ligation. In control studies, where a second ligature was placed proximal to and before the first to reduce blood to the distal constriction site substantially or totally, endothelial desquamation was found in only one of 14 animals, and the number of craters and balloons was significantly reduced. We suggest that endothelial damage and thrombus formation may occur at the site of focal arterial constriction even when the reduction in transluminal diameter is insufficient to alter substantially the rate of flow.
Diet and its relation to coronary heart disease and death in three populations.
Authors: Gordon T , Kagan A , Garcia-Palmieri M , Kannel W B , Zukel W J , Tillotson J , Sorlie P , Hjortland M
Published: June 2011

Baseline 24-hour dietary recalls from 16,349 men ages 45-64 years who had no evidence of coronary heart disease (CHD) were obtained in three prospective studies: the Framingham Study (859 men), the Honolulu Heart Study (7272 men) and the Puerto Rico Heart Health Program (8218 men). These men were followed for up to 6 years for the first appearance of CHD or death. Men who had a greater caloric intake or a greater caloric intake per kilogram of body weight were less likely to develop CHD manifest as myocardial infarction (MI) or CHD death, even though men of greater weight were more likely to develop CHD. This may reflect the benefit of greater physical activity. Men who consumed more alcohol were less likely to develop CHD, but more likely to die of causes other than CHD, particularly in the Honolulu study. In the Honolulu and Puerto Rico studies, but not in the Framingham study, men who consumed more starch were less likely to develop MI or CHD death. There was an inverse relation between starch intake and serum cholesterol, but it was too weak to explain fully the inverse starch-CHD association. There was also no evidence that the inverse relation between starch intake and incidence of CHD in the Honolulu and Puerto Rico studies was an indirect result of differences in fat intake. While the findings suggest additional areas for research, none of them would lead to an alteration of currently recommended preventive diets that emphasize lowering fat intake, because in isocaloric diets the logical way to balance a decreased fat intake is to increase the consumption of foods containing starch.
Effect of oral propranolol on rest, exercise and postexercise left ventricular performance in normal subjects and patients with coronary artery disease.
Authors: Marshall R C , Wisenberg G , Schelbert H R , Henze E
Published: June 2011

The effect of beta-adrenergic blockade with oral propranolol on resting, exercise and postexercise ventricular performance was evaluated using multiple-gated equilibrium cardiac blood and pool images in normal volunteers and patients with coronary artery disease. Propranolol produced no detectable effect on basal left ventricular function in normal subjects at doses producing intermediate (160 mg propranolol/day) and maximal (434 +/- 99 mg propranolol/day) beta blockade and in patients with coronary artery disease at clinically effective antianginal doses (162 +/- 47 mg propranolol/day). During exercise, a dose-related, negative inotropic effect was observed in normal subjects: 160 mg propranolol/day produced a small but statistically insignificant decline in exercise left ventricular performance, whereas maximal beta blockade significantly depressed the left ventricular response to exercise. In patients with coronary artery disease, propranolol's effect on exercise ventricular performance depended on the presence or absence of ischemic dysfunction during exercise. In patients with an ischemic functional response to exercise, propranolol significantly improved regional and global performance during and after exercise; in coronary artery disease patients with a normal response to exercise, propranolol had no significant effect on exercise and postexercise ventricular function. These results imply increased sensitivity to the effects of beta blockade in ischemic myocardium. In coronary artery disease patients with an abnormal response to exercise and in normal volunteers during beta blockade, propranolol's effect on exercise left ventricular performance was independent of changes in ventricular preload and after load related to heart rate and blood pressure.
Left ventricular function during sudden strenuous exercise.
Authors: Foster C , Anholm J D , Hellman C K , Carpenter J , Pollock M L , Schmidt D H
Published: June 2011

Strenuous exercise without warm-up has been shown to produce ischemia-like electrocardiographic (ECG) abnormalities in 60-70% of healthy subjects. These abnormalities appeared to be related to the development of an unfavorable myocardial supply/demand balance and, in chronically instrumented dogs, to transient decreases in coronary blood flow. A mechanism involving subendocardial ischemia has been proposed to explain the response to sudden strenuous exercise (SSE). To determine whether the response to SSE included the development of changes in myocardial pump performance typical of ischemia, left ventricular (LV) function at rest, during graded exercise and during SSE was evaluated in nine young (26.6 +/- 3.4 years), well-trained male volunteers using first-pass radionuclide angiography. During graded exercise, the LV ejection fraction increased from 66.9 +/- 9.4% at rest to 73.0 +/- 7.1% during peak exercise, and the LV ejection rate increased from 3.36 +/- 0.67 sec-1 at rest to 6.58 +/- 1.10 sec-1 during peak exercise. Segmental wall motion was normal in all studies. During SSE, the LV ejection fraction decreased in very subject, from an average 72.2 +/- 8.6% at rst to 57.3 +/- 8.1% during exercise. The LV ejection rate remained relatively constant (3.98 +/- 0.92 sec-1 at rest vs 4.33 +/- 0.74 sec-1 during SSE). No segmental wall motion abnormalities were observed during SSE; however, LV wall motion appeared to be diffusely hypokinetic during SSE. In contrast to previous reports, few ECG abnormalities were observed during SSE. These results support the hypothesis that subendocardial ischemia is an important mechanism in the response to SSE. However, the lack of ECG changes and segmental wall motion abnormalities and the relatively high absolute value of the LV ejection fraction suggest that if subendocardial ischemia occurs during SSE, it is attributable to physiologic rather than pathologic mechanisms.
Body surface distributions of repolarization potentials after acute myocardial infarction. II. Relationship between isopotential mapping and ST-segment potential summation methods.
Authors: Mirvis D M
Published: June 2011

Isopotential body surface distribution derived from 14 subjects with acute anterior and 14 patients with acute inferior myocardial infarction were studied to examine three possible difficulties with ST-segment summation methods as used for evaluation of infarction severity. First, recorded sums of potentials recorded from 150 electrodes placed on anterior and posterior thoracic surfaces and from five subsets of 42 electrodes located only on the left anterior precordium were compared. Lead subsets detected only one-half of total thoracic positivity in acute anterior infarction and the sums of potentials in these sets were significantly altered by small (approximately 1-1.5-inch) deviations in grid location. Second, differing isopotential distributions could yield nearly identical sums of potentials in left precordial electrode grids. Third, the effects of the wide variations in the normal ST-segment isopotential distribution were evaluated by studying 45 normal subjects and application of difference map and departure map and departure map techniques. The results illustrate the significant variation in potentials considered to be generated by the ischemic lesion caused by differences in control patterns. Thus, the recording of potential sums over limited torso areas, the attention to potential magnitudes rather than to distributions and the assumption that the normal ST segment is isoelectric represent significant problems in applying ECG methods to the quantitative evaluation of myocardial infarction.
Quantitative thallium-201 redistribution with a fixed coronary stenosis in dogs.
Authors: Leppo J , Rosenkrantz J , Rosenthal R , Bontemps R , Yipintsoi T
Published: June 2011

The redistribution of thallium-201 (201Tl) after coronary vasodilation was studied in 14 dogs with a proximal stenosis of the left circumflex coronary artery that did not reduce basal flow but attenuated reactive hypermia. During an 8-10-minute i.v. infusion of adenosine, radioactive microspheres and 201Tl were injected into the left atrium. Sequential cardiac scintiscans and microsphere injections permitted subsequent determination of coronary blood flow during the redistribution of 201Tl. After 15-220 minutes of observation, the dogs were killed and the hearts removed for the measurement of the activity of 201Tl and the radioactive microspheres in the normal (left anterior descending coronary artery [LAD]) and flow-restricted (left circumflex coronary artery [LCX]) regions. The ratios of the activity in LAD/LCX for microspheres (TRmic) and for 201Tl (RT1) were compared with the activity ratio determined from the scintiscan (Rscan). Rmic for the microsphere simultaneously injected with 201Tl can be compared with the initial Rscan, which showed a significant hourly decrease from an initial value of 1.26 +/- 0.12 to a mean final value of 1.02 +/- 0.09 by 3-4 hours. The final Rscan (mean 1.07 +/- 0.10) in each experiment also correlated significantly (r = 0.854) with the final true myocardial RT1 (mean 1.26 +/- 0.25). Rscan underestimated Rmic (average 2.25 +/- 0.48) when both 201Tl and microspheres were simultaneously injected; Rscan also underestimated RT1, but the directional changes were similar. A further analysis of the Rmic, Rscan and RT1 in two groups of dogs with either relatively high or low coronary flow during adenosine infusion suggests that the net loss of cellular 201Tl from the normal scintigraphic area is the mechanism underlying the resolution of these initial defects.
Postural hypotension and tachycardia during hydralazine--isosorbide dinitrate therapy for chronic heart failure.
Authors: Massie B , Kramer B , Haughom F
Published: June 2011

Supine and upright hemodynamic measurements were performed in 10 patients with chronic congestive heart failure, before and during vasodilator therapy with hydralazine and isosorbide dinitrate. This combination of drugs produced significant improvement in supine hemodynamic measurements, with the pulmonary capillary wedge pressure decreasing from 26 +/- 5 to 18 +/- 5 mm Hg (mean +/- SD, p less than 0.01) and stroke volume index increasing from 25 +/- 6 to 39 +/- 6 ml/m2 (p less than 0.01), without any significant change in heart rate (HR) or mean arterial pressure (MAP). However, with the patients upright, HR rose significantly (87 +/- 17 to 99 +/- 17 beats/min, p less than 0.05) and MAP fell (84 +/- 10 to 66 +/- 11 mm Hg, p less than 0.001) compared with measurements before treatment. These patients also exhibited potentially deleterious postural changes in HR, MAP, cardiac output, stroke volume index and stroke work index during therapy with the combination of hydralazine and isosorbide dinitrate. Although diuretic therapy (which had been withheld for 12 hours in eight subjects but only for 6 hours in two others) may have played a role in producing these changes, postural hypotension or tachycardia was not noted before vasodilator therapy or during therapy with nitrates or hydralazine. Repeat catheterization after 3 months in six patients revealed a lessening of the postural effects. These findings indicate the need to perform upright as well as supine hemodynamic measurements during the initiation of vasodilator therapy and suggest the need for particular caution in patients with ischemic heart disease.
Transthoracic resistance in human defibrillation. Influence of body weight, chest size, serial shocks, paddle size and paddle contact pressure.
Authors: Kerber R E , Grayzel J , Hoyt R , Marcus M , Kennedy J
Published: June 2011

Successful defibrillation depends on delivery of adequate electrical current to the heart; one of the major determinants of current flow is transthoracic resistance (TTR). To study the factors influencing TTR, we prospectively collected data from 44 patients undergoing emergency defibrillation. Shocks of 94-450 J delivered energy were administered from specially calibrated Datascope defibrillators that displayed peak current flow, thereby permitting determination of TTR. Shocks were applied from standard (8.5-cm diameter) or large (13 cm) paddles placed anteriorly and laterally. First-shock TTR ranged from 15-143 omega. There was a weak correlation between TTR and body weight (r = 0.45, p less than 0.05) and a stronger correlation between TTR and chest width (r = 0.80, p less than 0.01). Twenty-three patients who were defibrillated using standard 8.5-cm paddles had a mean TTR of 67 +/- 36 omega (+/- SD), whereas 21 patients who received shocks using paddle pairs with at least one large (13 cm) paddle had a 21% lower TTR of 53 +/- 24 omega (p = 0.05, unpaired t test). Ten patients received first and second shocks at the same energy level; TTR declined only 8%, from 52 +/- 19 to 48 +/- 16 omega (p less than 0.01, paired t test). In closed chest dogs, shocks were administered using a spring apparatus that regulated paddle contact pressure against the thorax. Firmer contact pressure caused TTR to decrease 25%, from 48 +/- 22 to 36 +/- 17 omega (p less than 0.01, paired t test). Thus, human TTR varies widely and is related most closely to chest size. TTR declines only slightly with a second shock at the same energy level. More substantial reductions in TTR and declines only slightly with a second shock at the same energy level. More substantial reductions in TTR and increases in current flow can be achieved by using large paddles and applying firm paddle contact pressure.
Factors affecting real-time, cross-sectional echocardiographic imaging of perimembranous ventricular septal defects.
Authors: Canale J M , Sahn D J , Allen H D , Goldberg S J , Valdes-Cruz L M , Ovitt T W
Published: June 2011

Recent studies suggest good prospective accuracy for two-dimensional echocardiographic imaging of ventricular septal defects (VSD). We obtained two-dimensional images with high-frequency, high-resolution scanners from 36 patients proved by cardiac catheterization to have perimembranous VSD. In 20 patients, the VSD was an isolated lesion and in 16 it was associated with other forms of heart disease. VSDs were imaged in long-axis, apical four-chamber and subcostal echocardiographic views. The smallest VSD imaged was 2 mm in diameter on echo; the largest, 23 mm. The imaged size of VSDs was larger at end-diastole than at end-systole by paired t test on all views (all p less than 0.005). VSD size also varied between views, with no predictive relationship except between apical and subcostal four-chamber views in diastole (r = 0.71, p less than 0.005). This agreed with qualitative direct observations of an ellipsoid or irregularly shaped VSD in operated patients. Echocardiographically measured VSD size normalized for either aortic root size or for patient weight could be used to separate isolated VSDs with large shunts (Qp/Qs greater than 2:1) from those with small shunts. Review of 250 two-dimensional echocardiographic studies from patients proved not to have a VSD revealed 28 planes of imaging with false-positive VSD. None of the false-positive VSDs was imaged consistently on all views. Additionally, a "T" artifact (broadening of septal edges around a VSD) has been found to be a reliable marker of true VSD imaging. To best quantify VSD size and to avoid false-positive diagnoses, it is necessary to use multiple views and to consider the marked changes in VSD size that occur between diastole and systole.
Quantitative detection of regional left ventricular contraction abnormalities by two-dimensional echocardiography. II. Accuracy in coronary artery disease.
Authors: Parisi A F , Moynihan P F , Folland E D , Feldman C L
Published: June 2011

The quantitative approaches to the assessment of regional left ventricular (LV) function described in the preceding paper were applied in a well-defined population of patients with coronary artery disease. Two groups were chosen by electrocardiographic and angiographic criteria: group 1 had infarction and regional wall motion abnormalities and group 2 had no infarction and normal wall motion. Sensitivity to detect wall motion defects, specificity to correctly categorize normal segments, and overall predictive accuracy were evaluated for each two-dimensional echocardiographic approach. In addition, the ability of each method to localize regional contraction defects properly was evaluated. Area methods yielded better predictive accuracy than linear methods (87-95% vs 76-84%). No significant differences in accuracy were noted between quadrant and octant approaches. The fixed external-axis system was superior to a floating one for localizing contraction defects. We conclude that an area-based method, using a fixed-axis system and either octant or quadrant image subdivision, provides the best combination of predictive accuracy in categorizing LV segments as normal or abnormal and the greatest ability to localize LV regional abnormalities.
Clinical and angiographic predictors of operative mortality from the collaborative study in coronary artery surgery (CASS).
Authors: Kennedy J W , Kaiser G C , Fisher L D , Fritz J K , Myers W , Mudd J G , Ryan T J
Published: June 2011

Fifteen institutions participating in the Collaborative Study in Coronary Artery Surgery (CASS) have performed isolated coronary artery bypass surgery upon 6630 patients (1061 women and 5569 men) for coronary artery disease. The overall operative mortality (OM) was 2.3% (range 0.3-6.4%). Mortality increased with age, from 0 in the group 20-29 years old to 7.9% in the group 70 years and older. OM was higher for women in each group, ranging from 2.8% for ages 30-39 years to 12.3% for age 70 years and older (0.8% and 5.8% for men). Clinical manifestations of congestive heart failure were associated with increased OM. Mortality was 1.4% in one-vessel, 2.1% in two-vessel and 2.8% in three-vessel disease (diameter narrowing greater than or equal to 70%). Among 1019 patients with left main coronary artery (LMCA) stenosis, OM ranged from 1.6% in patients with mild stenosis and a right-dominant system to 25% in patients with severe (greater than or equal to 90%) stenosis and left dominance. OM varied with ejection fraction (EF) (1.9% for EF greater than or equal to 50% to 6.7% for EF less than 19%) and left ventricular wall motion score (1.7% for least abnormal to 9.1% for most abnormal). For elective surgery, OM was 1.7%, for urgent surgery 3.5%, and for emergency surgery 10.8%. Mortality was 40.0% among 30 patients with severe LMCA stenosis who underwent emergency revascularization. Advanced age, female sex, symptoms of heart failure, LMCA stenosis, impaired left ventricular function and nonelective surgery are associated with a higher OM. These factors should be considered in the selection of patients for coronary artery surgery.
Prevention of nifedipine of abnormal coronary vasoconstriction in patients with coronary artery disease.
Authors: Gunther S , Green L , Muller J E , Mudge G H , Grossman W
Published: June 2011

The hemodynamic and myocardial metabolic responses to the cold pressor test were studied in 15 patients with coronary artery disease and stable exertional angina. Every patient had abnormal coronary vasoconstriction during a control cold pressor test, even though 14 were receiving propranolol and 12 were receiving long acting nitrates. Mean coronary vascular resistance for the group increased 18 +/- 6% (SD) (from 0.80 +/- 0.12 to 0.94 +/- 0.20 mm Hg/ml/min, p less than 0.05); coronary sinus blood was unchanged, and the arterial-coronary sinus oxygen difference widened significantly (from 11.5 +/- 1.2 to 12.3 +/- 1.2 ml/100 ml, p less than 0.05). Four patients developed angina, accompanied in each instance by a negative arterial-coronary sinus lactate difference. After the administration of nifedipine (10 mg buccally) in 10 patients, the coronary vascular responses to a repeat cold pressor test were normal in each patient. Mean coronary sinus blood flow increased 27 +/- 12% (from 122 +/- 32 to 153 +/- 35 ml/min, p less than 0.05), coronary vascular resistance decreased 10 +/- 6% (from 0.85 +/- 0.16 to 0.76 +/- 0.16 mm Hg/ml/min, p less than 0.05), and the arterial-coronary sinus oxygen difference was unchanged. No patient experienced angina. The hemodynamic and coronary vascular responses to a repeat cold pressor test in five patients given placebo were unaltered from control responses. The protective effects of nifedipine were unaccompanied by any change in mean arterial pressure, left ventricular filling pressure or myocardial oxygen consumption either at rest or in response to the cold pressor test. Nifedipine appears to exert a selective antivasoconstrictor effect on the coronary vasculature.
Effect of negative intrathoracic pressure on left ventricular outflow tract obstruction in muscular subaortic stenosis.
Authors: Buda A J , MacKenzie G W , Wigle E D
Published: June 2011

To study the effect of respiration and negative intrathoracic pressure on the left ventricular outflow tract gradient in patients with muscular subaortic stenosis, we studied nine patients using various respiratory maneuvers at the time of cardiac catheterization. Deep inspiration decreased the left ventricular outflow tract gradient from 60 +/- 11 to 34 +/- 6 mm Hg (p less than 0.01) and decreased the left ventricular ejection time (corrected for heart rate) from 0.42 +/- 0.01 to 0.38 +/- 0.01 second (p less than 0.001). The Müller maneuver decreased the left ventricular outflow tract gradient from 69 +/- 13 to 7 +/- 3 mm Hg (p less than 0.001) and decreased the corrected left ventricular ejection time from 0.42 +/- 0.02 to 0.24 +/- 0.01 second (p less than 0.01). In keeping with this amelioration of left ventricular outflow tract obstruction, echocardiography showed a reduction or abolition of the systolic anterior motion of the anterior mitral leaflet, and auscultatory and phonocardiographic studies revealed a decrease or abolition of the apical systolic murmur. These findings indicate that negative intrathoracic pressure reduced the left ventricular outflow tract gradient in muscular subaortic stenosis. We believe that negative intrathoracic pressure produced these changes by increasing left ventricular afterload through an increase in left ventricular transmural pressure, resulting in a decrease in the left ventricular outflow tract obstruction. These observations provide an explanation for the decrease in pressure gradient that occurs on inspiration in patients with muscular subaortic stenosis.
Correlation of the width of the QRS complex with the pathologic anatomy of the cardiac conduction system in patients with chronic complete atrioventricular block.
Authors: Ohkawa S , Hackel D B , Ideker R E
Published: June 2011

A study correlating the electrocardiographic findings and the histology of the atrioventricular (AV) conduction system was carried out in 14 cases with chronic complete AV block and in 13 cases without chronic complete AV block. Patients with chronic complete AV block were divided into two groups, based on the width of the QRS complex. The QRS complexes were narrow (less than 0.12 second) in four cases (group 1) and wide (greater than or equal to 0.12 second) in 10 cases (group 2). In group 1, the main lesion was located in the penetrating portion of His bundle (Hisp) in one heart, in the branching portion of the His bundle (Hisb) in another and in the combined regions of Hisb and the left bundle branch in two. Three of the four cases in group 1 had idiopathic fibrosis of the conduction system and one had calcific nodules in the central fibrous body. In group 2, the main lesion was located in Hisb in two cases, in the combined regions of Hisb and the right bundle branch in one, in the Hisb and in the bilateral bundle branches in two, and in the bilateral bundle branches in five. All cases in group 2 were of the idiopathic type, except case 5, which had calcific aortic stenosis. In 13 cases without chronic complete AV block the AV conduction system was histologically normal, except for slight-to-moderate aging changes in the His bundle or the bundle branches. Lesions of the Hisb, which is believed to be the "distal His" electrophysiologically, may induce complete AV block with narrow or wide QRS complexes, depending upon the severity of the lesions in Hisb or adjacent bundle branches.
Surface recording of His-Purkinje activity on an every-beat basis without digital averaging.
Authors: Flowers N C , Shvartsman V , Kennelly B M , Sohi G S , Horan L G
Published: June 2011

Efforts to record evidence of electrical activity from the body surface originating in the His bundle or bundle branches have been reported since 1973. Almost exclusively, these techniques have required digital averaging of 50-100 sequential cardiac cycles. For immediate diagnostic, therapeutic and prognostic application, recording on an every-beat basis is highly desirable. This is especially important in instances of changing atrioventricular conduction, arrhythmias or less-than-constant RR intervals. Our object has been to develop a system for more nearly optimal noise reduction, to avoid the disadvantages of serial signal averaging, and to be able to record His-Purkinje activity in man on an every-beat basis. Using multiple parallel inputs wih linear amplification, additional logarithmic amplification, some bandpass filtering, and a logic circuit that ultimately examines and accepts or rejects a deflection as "true" signal, we can record, in most instances, on a beat-by-beat basis, this very valuable component of the cardiac electrical cycle.
Natural history of chronic second-degree atrioventricular nodal block.
Authors: Strasberg B , Amat-Y-Leon F , Dhingra R C , Palileo E , Swiryn S , Bauernfeind R , Wyndham C , Rosen K M
Published: June 2011

This report details our experience with documented chronic second-degree atrioventricular (AV) nodal block (proximal to His [H]) in 56 patients. Forty-six men (82%) and 10 women (18%), ages 18-87 years, were studied. Nineteen of the patients (34%) had no organic heart disease (including seven trained athletes) and 37 (66%) had organic heart disease. ECGs in all patients demonstrated episodes of type I second-degree block; five patients also had periods of 2:1 block. Prospective follow-up patients with no organic heart disease (157-2280 days, mean 1395 +/- 636 days) revealed one patient with clear indication for permanent pacing because of bradyarrhythmic symptoms (permanently placed on day 220 of follow-up). Two patients died nonsuddenly. In patients with organic heart disease (prospective follow-up of 60-2950 days, mean 1347 +/- 825 days), pacemakers were implanted in 10 patients, primarily for treatment of congestive heart failure in eight and syncope in two. Sixteen patients died -- three suddenly, seven with congestive heart failure, two of an acute myocardial infarction and four of causes unrelated to cardiac disease. In summary, chronic second-degree AV nodal block has a relatively benign course in patients without organic heart disease. In patients with organic heart disease, prognosis is poor and related to the severity of underlying heart disease.
The effect of swimming on patients with ischemic heart disease.
Authors: Magder S , Linnarsson D , Gullstrand L
Published: June 2011

Swimming is frequently recommended for cardiac rehabilitation, but little is known of its physiologic consequences in ischemic heart disease. Eight males who had had a myocardial infarction 8-17 months before the study were exercised to exhaustion or angina with 10 W/min-1 ramp on a cycle ergometer in sitting and supine positions. Oxygen uptake (VO2) was continuously measured to monitor the physiologic power requirement. All eight patients were taking beta blockers and four were taking digoxin. During sitting cycling, angina occurred in four and ST depression in five; during supine cycling, angina occurred in five and ST depression in six. VO2 was then measured while they swam at their own comfortable speed (mean 0.43 m/sec-1) in a swimming flume at water temperatures of 25.5 degrees C and 18 degrees C. In six, the water speed was gradually increased until they were limited by symptoms. Comfortable swimming at 25.5 degrees C was 87% (1.28 1/min-1) and at 18 degrees C 89% (1.30 1/min-1) of sitting peak VO2, while heart rates were 92% and 91% respectively. The mean peak VO2 and heart rate did not differ significantly between bicycle and swim tests (peak VO2 sitting 1.49 +/- 0.23, supine 1.42 +/- 0.24, 25.5 degrees C 1.60 +/- 0.17, 18 degrees C 1.52 +/- 0.19 1/min-1). Only two patients reported angina while swimming in warm water and one in cold water, although ST depression occurred in six in both swims. The subjective comfort and large muscle groups involved make swimming a good exercise, but the high relative energy cost and failure to identify ischemic symptoms indicate caution in cardiac patients, especially if their swimming skills are poor.
Digoxin sensitivity in amyloid cardiomyopathy.
Authors: Rubinow A , Skinner M , Cohen A S
Published: June 2011

Digoxin (5 mg/ml) was added to 10-mg and 20-mg pellets of purified primary and secondary amyloid fibrils, a normal human liver and heart homogenate and a homogenate from the heart of a patient with amyloid cardiomyopathy who had not received digitalis. After centrifugation, the supernatants were recovered and assayed for digoxin concentrations. Aliquots from the sediments were studied for the presence of digoxin, using rabbits antidigoxin antiserum and an indirect immunofluorescent technique. The results showed that 0.11--0.13 ng/ml of digoxin bound per milligram of fibrils and could not be separated by repeated washings. Elution with citrate or changes in the pH of the buffer. Immunofluorescent studies demonstrated diffusely bright immunofluorescence with the fibril preparation and amyloid heart homogenate when reacted with digoxin and digoxin-specific antiserum. These studies demonstrate that isolated amyloid fibrils bind digoxin and suggest that this interaction may play some role in the sensitivity to digitalis that has been observed in some patients with amyloid cardiomyopathy.
Premature ventricular complexes in the absence of identifiable heart disease.
Authors: Kostis J B , McCrone K , Moreyra A E , Gotzoyannis S , Aglitz N M , Natarajan N , Kuo P T
Published: June 2011

To define the prevalence, frequency and characteristics of premature ventricular complexes (PVCs) in adults free of recognizable heart disease, we performed 24-hour ambulatory electrocardiography on 101 subjects (51 men and 50 women, mean age 48.8 years) in whom physical examination, chest x-ray, ECG, echocardiogram, maximal exercise stress test, right- and left-heart catheterization and coronary arteriography were normal. Thirty-nine subjects had at least 1 PVC/24 hours, but only four had more than 100 PVCs/24 hours and fewer than five had more than five PVCs in any given hour. The probability of having at least 1 PVC/24 hours increased with age (chi square = 11.789, p = 0.019). The number of PVCs/24 hours was also positively associated with age (4 = 0.33, p = 0.001). These was no consistent relationship between the presence or number of PVCs/24 hours and sex, blood pressure, weight, height, body mass index, serum potassium or calcium, cholesterol and triglyceride, hemoglobin, the ingestion of coffee, tea or alcohol, and cigarette smoking. Four subjects had multiform PVCs, two of whom had early PVCs.
Exercise-induced ST-segment elevation in leads V1 or aVL. A predictor of anterior myocardial ischemia and left anterior descending coronary artery disease.
Authors: Dunn R F , Freedman B , Kelly D T , Bailey I K , McLaughlin A
Published: June 2011

Exercise-induced ST-segment elevation in leads V1 and/or aVL in the absence of anterior Q waves occurred in 46 of 190 patients (24%) who underwent 12-lead exercise electrocardiography with thallium-201 myocardial perfusion imaging and coronary arteriography. Significant left anterior descending coronary artery (LAD) disease was present in 38 of 46 patients (83%) with V1/aVL ST evaluation and in 72 of 144 patients (50%) without V1/aVL ST elevation (p less than 0.0005). Anterior myocardial ischemia, indicated by reversible anterior perfusion defects on thallium scanning, was present in 40 of 46 patients (87%) with V1/aVL ST elevation and in 25 of 144 patients (17%) without V1/aVL ST elevation (p less than 0.0005). Exercise ST elevation in V1/aVL was detected in 38 of 110 of the patients (35%) with LAD disease, for a specificity of 90%, and in 40 of 65 of the patients (62%) with anterior myocardial ischemia, for a specificity of 95%. We conclude that during 12-lead exercise electrocardiography, ST-segment elevation in V1 and/or a VL in the absence of anterior Q waves predicts anterior myocardial ischemia and LAD disease.
Asystolic episodes during pacemaker implantation.
Authors: Astrinsky E A , Furman S , Florio J
Published: June 2011

During normal rate programming of a pulse generator from slower to more rapid rates, intervals of output impulse suppression lasting 2 seconds plus the newly programmed interval to a maximum of 3.935 seconds are possible, and are a result of the pulse interval control system. These occur if programming falls within the susceptible window (the period between the existing interval and the new one) but will not take place if the programming command is given immediately after an output pulse. Four incidents with resulting ventricular asystole of up to 2.8 seconds are documented and explained. No significant clinical complications were observed.
Visualization of cardiac valve motion in man during external chest compression using two-dimensional echocardiography. Implications regarding the mechanism of blood flow.
Authors: Werner J A , Greene H L , Janko C L , Cobb L A
Published: June 2011

Five patients who underwent cardiopulmonary resuscitation (CPR) were studied by two-dimensional echocardiography to assess valve motion. The mitral valve remained open throughout the entire compression-release cycle of CPR. The aortic valve opened during the compression phase of CPR and closed during the release phase. The pulmonic valve moved toward the closed position during the compression phase and the valve leaflets opened during release. Tricuspid valve leaflets never completely apposed, even during maximum chest compression, and they were widely open during release. Left ventricular dimensions did not change appreciably during CPR. These findings support the theory that forward blood flow during CPR depends on a generalized increase in intrathoracic pressure and not on direct compression of the heart itself. The left heart appears to act as a conduit for passage of blood, and mitral valve closure is not necessary for forward blood flow during CPR.
Mitral valve prolapse: a consistent manifestation of type IV Ehlers-Danlos syndrome. The pathogenetic role of the abnormal production of type III collagen.
Authors: Jaffe A S , Geltman E M , Rodey G E , Uitto J
Published: June 2011

To evaluate whether abnormal production of type III collagen, the characteristic biochemical feature of patients with the type IV Ehlers-Danlos syndrome, consistently predisposes to mitral valve prolapse, we evaluated the family of a proband with classic type IV Ehlers-Danlos syndrome. Production of type III collagen was assessed with the use of cultured skin fibroblasts. Mitral valve prolapse was detected by M-mode and two-dimensional echocardiography. Biochemical abnormalities in the production of type III collagen and echocardiographic findings of mitral valve prolapse were completely concordant. All patients with abnormal production of type III collagen had mitral valve prolapse and all subjects with normal production of type III collagen had entirely normal echocardiograms. Six of the eight patients with abnormal production of type III collagen had subtle cutaneous abnormalities. The consistent association of abnormal production of type III collagen and mitral valve prolapse in this family suggests that this abnormality of collagen may give rise to mitral valve prolapse.
Effect of sulfinpyrazone on ventricular fibrillation during acute myocardial ischemia.
Authors: Moschos C B , Escobinas A J , Jorgensen O B , Regan T J
Published: June 2011

In patients treated with sulfinpyrazone, an apparent reduction in the incidence of sudden death and presumed ventricular fibrillation has been reported. Using an intact animal model without microcirculatory thrombosis, we studied the effects of sulfinpyrazone on ischemic myocardium in 58 anesthetized dogs divided into three groups: control untreated (n =24), group 1 (n = 16), treated daily with 300 mg of sulfinpyrazone for 7 days, and group 2 (n = 18), treated daily with 300 mg of sulfinpyrazone for 7 days but omitting treatment on day 8. Although consistent hemodynamic differences were not apparent, the degree of injury determined by ECG mapping was significantly lower in group 1. The incidence of fibrillation was 54% for control and 0% in group 1. Group 2 had a 44% incidence, suggesting a limited duration of action. The apparent absence of microcirculatory thrombosis in this model suggests other mechanisms of action. A significantly smaller increase in tissue water and Na+ and smaller loss of K+ in group 1 may have contributed to the lower incidence of fibrillation, perhaps through selective prostaglandin inhibition.
Role of Mahaim fibers in cardiac arrhythmias in man.
Authors: Gallagher J J , Smith W M , Kasell J H , Benson D W , Sterba R , Grant A O
Published: June 2011

Twelve patients with evidence of Mahaim fibers are reported, six with nodoventricular (NV) fibers and six with fasciculoventricular (FV) fibers. All patients with NV fibers had left bundle branch block morphology, and a sustained reentrant tachycardia with this morphology was proved in each case. In three of the six, ventriculoatrial dissociation occurred during tachycardia. We postulate that the mechanism of this tachycardia is a macroreentry circuit using the NV fiber for the antegrade limb and the His-Purkinje system with a portion of the atrioventricular node for the retrograde limb. ECGs of patients with FV fibers were varied, suggesting a functional relation to the right or left side of the septum. No direct relationship of FV fibers to observed arrhythmias could be found.
Clinical and experimental studies on electromechanical dissociation.
Authors: Vincent J L , Thijs L , Weil M H , Michaels S , Silverberg R A
Published: June 2011

Electromechanical dissociation (EMD) is the most frequent cause of unsuccessful cardiac resuscitation in critically ill patients. In a clinical study of cardiac arrest, including 54 episodes in 50 fully monitored patients, 14 episodes of ventricular fibrillation were observed and seven were reversed. In the remaining 40 instances, 36 cases of EMD were initially observed. Four patients had asystole. None of the patients with EMD or asystole were successfully resuscitated. For objective study of EMD and its treatment, we developed an experimental model in which ventricular fibrillation was induced in mechanically ventilated dogs. EMD was predictably observed when, after an interval of 120 seconds, ventricular fibrillation was reversed with an external countershock. Neither metabolic acidosis nor metabolic alkalosis modified the incidence of EMD. A few dogs were pretreated with glucose-insulin-potassium or pharmacologic doses of methylprednisolone, but this did not clearly reduce the incidence of EMD. However, the onset of EMD was delayed when the body temperature of the animal was spontaneously reduced.
Real-time, two-dimensional echocardiographic features of pacemaker perforation.
Authors: Gondi B , Nanda N C
Published: June 2011

Five patients (four adults and one child) with clinically suspected myocardial perforation by temporary transvenous pacemakers were studied by real-time, two-dimensional echocardiography. In three patients, the catheters were visualized passing through the right ventricular apical wall with the tip located outside the cardiac border. In one patient the catheter perforated the atrioventricular septum and entered the left ventricle with the tip lodged against the posterior wall. In another patient, the catheter had partially penetrated the ventricular septum near the apex. Pericardial effusion was observed in two patients, in one of whom it was localized to the site of perforation. No patient had evidence of cardiac tamponade. In four patients, the catheters were withdrawn under echocardiographic visualization and the catheter tips could be seen moving from the abnormal locations back into the right-heart chambers. Perforation was verified at autopsy in two patients, including one in whom the catheter was not withdrawn. Real-time, two-dimensional echocardiography appears to be valuable in the diagnosis of pacemaker perforation.
Relationship between plasma levels of procainamide, suppression of premature ventricular complexes and prevention of recurrent ventricular tachycardia.
Authors: Myerburg R J , Kessler K M , Kiem I , Pefkaros K C , Conde C A , Cooper D , Castellanos A
Published: June 2011

We compared the relationship between plasma levels of procainamide and suppression or prevention of various forms of ventricular arrhythmias in 18 patients, six of whom had premature ventricular complexes (PVCs) during acute myocardial infarction (AMI), six of whom had PVCs in the setting of stable chronic ischemic heart disease (CIHD), and six of whom had recurrent symptomatic ventricular tachycardia (VT) with chronic PVCs between episodes of VT. The mean plasma level of procainamide required for 85% suppression of PVCs in the AMI patients was 5.0 +/- 0.5 micrograms/ml, while that required for the CIHD patients was 9.3 +/- 0.7 micrograms/ml (p less than 0.05). The mean plasma level required for prevention of spontaneous episodes of symptomatic sustained tachycardia in the VT group was 9.1 +/- 3.4 micrograms/ml, while the mean level required for 85% suppression of PVCs in the same patients was 14.9 +/- 3.8 micrograms/ml (p less than 0.01). In the VT group, PVC frequency was decreased by a mean of only 36% (range 11-63%) at plasma levels of procainamide sufficient to prevent spontaneous VT. The relationship between plasma levels of procainamide and PVC suppression appears to be different in AMI and CIHD patients; furthermore, a high degree of PVC suppression is not a necessary endpoint of antiarrhythmic therapy when attempting to protect patients against recurrent symptomatic VT.