Left atrial appendage aneurysm with associated anomalous pulmonary venous drainage.
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Aged↗
Biomedical subjects
P J Scanlon
Publications and source records attributed to P J Scanlon.
Mechanisms responsible for countershock-induced ventricular tachycardia in the intact canine heart.
To determine the mechanism for postcountershock ventricular ectopy, internal and external shocks were delivered to 20 anesthetized dogs. Shock energies of 25 and 50 joules were employed internally while 100 and 200 joules were delivered externally. Experiments were performed in both the presence and absence of a nearly toxic dose of ouabain. All shocks resulted in the occurrence of nonsustained (less than 15 seconds) ventricular tachycardia. When bursts of rapid ventricular pacing were synchronized with a shock, the pacing stimuli invariably captured the ventricles and overdrove the shock-induced ventricular tachycardia. However, the burst pacing never appeared to break a tachycardia, since the termination of pacing was followed immediately by the resumption of the shock-induced ventricular tachycardia. The presence of ouabain did not alter the response of the ventricles to postshock burst pacing. Administration of verapamil (0.5 mg/kg) had no effect on the duration of shock-induced ventricular arrhythmia. Elevation of the serum potassium level to 8.5 +/- 0.6 mEq/L drastically reduced the duration of postshock ventricular tachycardia in both the presence and absence of ouabain. The results suggest that postshock ventricular ectopy results from an abnormality of impulse initiation rather than reentry.
Animals↗
The effects of elevated intracranial pressure on the canine electrocardiogram.
Striking electrocardiographic abnormalities have been noted in some patients with central nervous system injury. To study the relationship between the electrocardiogram and intracranial pressure, intracranial pressure was elevated in 14 open chest pentobarbital-anesthetized dogs. The right vagus was stimulated to produce sinus slowing and the right atrium was paced at a constant cycle length fast enough to prevent arrhythmias and maintain heart rate constant (750 msec in 11 dogs and 600 msec in three dogs). In nine dogs, intracranial pressure was sequentially elevated to 100, 150, and 200 mmHg. Systolic arterial blood pressure consistently rose to exceed intracranial pressure (P less than 0.005). At a pressure of 150 and 200 mmHg, mean QT intervals shortened significantly in recorded leads II, X, Y, and Z from 0.01). T wave changes were also noted that consisted of increasing positivity in leads II, X, and Y and increasing negativity in lead Z. To delinate the role of the sympathetic nervous system, an additional five dogs were subjected to an intracranial pressure of 200 mmHg before and after bilateral stellate ganglionectomy and timolol (0.1 mg/kg IV). Elimination of sympathetic influences did not significantly alter the electrocardiographic effects of elevated intracranial pressure. Thus, intracranial hypertension results in significant QT shortening and T wave changes that are not entirely mediated by the sympathetic nervous system.
Animals↗
The effect of sodium on the fibrillatory propensity of nonionic contrast media.
Removing sodium from standard ionic contrast media markedly increases the incidence of ventricular fibrillation in patients undergoing coronary angiography. Newer nonionic contrast media, iopamidol, iohexol, and ioversol contain only trace amounts of sodium. To determine whether sodium attenuates or potentiates ventricular fibrillation from nonionic contrast media, we measured the prolongation in QT interval and performed programmed electrical stimulation with one, two and three extra ventricular stimuli in 40 dogs during 4-mL intracoronary injections of iopamidol, iohexol, and ioversol. Solutions of each contrast medium with added NaCl at concentrations of 0.225%, 0.45%, and 0.9% were compared with standard contrast media. The addition of NaCl markedly increased the amount of QT interval prolongation produced by each contrast medium. With iopamidol, the amount of QT interval prolongation was 40 +/- 11 msec with standard iopamidol, but was 58 +/- 11 msec with 0.225% NaCl/iopamidol, 84 +/- 17 msec with 0.45% NaCl/iopamidol, and 132 +/- 42 msec with 0.9% NaCl/iopamidol (P less than .001). Similar results were seen with iohexol and ioversol. Ventricular fibrillation was difficult to induce with standard solutions of these agents (even with three extra stimuli), but became progressively easier to induce when NaCl was added. Three extra stimuli produced ventricular fibrillation in zero of 11 dogs with standard iopamidol, zero of 11 with 0.225% NaCl/iopamidol, three of 11 with 0.45% NaCl/iopamidol, and eight of 11 with 0.9% NaCl/iopamidol (P less than .001). Similar results were observed with iohexol and ioversol. The addition of choline chloride or dextrose did not increase ventricular fibrillation and QT interval prolongation. It is concluded that standard preparations of nonionic contrast media have a very low fibrillatory propensity.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Acetylcholine release by a stimulus train lowers atrial fibrillation threshold.
This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.
Acetylcholine↗
Beta blockers and the sensitivity of the thallium treadmill test.
The effect beta blockers (BB) may have on the sensitivity of the thallium treadmill test (Th-TMT) is controversial. The purpose of this study was to test the hypothesis that BB decrease the sensitivity of the Th-TMT. Two hundred three patients over a two-year period were identified who satisfied the following criteria. All had symptom-limited upright treadmill exercise tests with stress and redistribution thallium imaging, as well as coronary angiography within two months of the Th-TMT. Of 58 patients with CAD not on BB, 52 had an abnormal Th-TMT scan (sensitivity 90 percent). In comparison, the sensitivity of the Th-TMT scan in the 88 patients with CAD receiving BB was 76 percent (p less than 0.05). We conclude that BB may significantly decrease the sensitivity of the Th-TMT. Physicians should fully appreciate the higher false negative rate (24 vs 10 percent) for patients on BB and consider cautious withdrawal prior to diagnostic studies.
Adrenergic beta-Antagonists↗
Successful reversal of acute cardiac allograft rejection with OKT*3 monoclonal antibody.
The efficacy of OKT*3 monoclonal antibody in reversing acute cardiac allograft rejection was investigated in 10 cardiac transplant recipients aged 5 to 57 years (mean 34 +/- 18) and treated with the same induction and maintenance immunosuppression. Serial endomyocardial biopsies, right heart catheterization, and echocardiograms were performed for rejection surveillance. After intensified immunosuppression with equine antithymocyte globulins and steroids, nine patients showed persistent rejection (lymphocytic infiltration and myocyte necrosis). Conventional immunosuppression was contraindicated in one patient. OKT*3 (5 mg by intravenous push daily for 14 days) resulted in complete resolution of rejection in nine of 10 patients (90%). After therapy with OKT*3 mean right atrial and pulmonary arterial wedge pressure were significantly lower (9.1 +/- 4.0 vs 4.8 +/- 2.0 mm Hg and 13.4 +/- 4.3 vs 8.0 +/- 3.3 mm Hg, respectively; p less than .05). Cardiac index was doubled in two patients with rejection-induced cardiac dysfunction (1.5 vs 3.2 and 1.6 vs 2.7 liters/min/m2). Only two patients developed antibodies to OKT*3. Fever, nausea and headache occurred with the first three doses of OKT*3 and did not recur. One patient developed aseptic meningitis. OKT*3 effectively reverses refractory cardiac allograft rejection before the development of irreversible graft dysfunction. Patients who do not develop antibodies to OKT*3 can be retreated with this drug. Adverse reactions to OKT*3 are self-limited.
Acute Disease↗
Rejection of the transplanted heart.
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ABO Blood-Group System↗
Effects of indomethacin on coronary hemodynamics, myocardial metabolism and anginal threshold in coronary artery disease.
The effects of orally administered indomethacin or placebo on coronary hemodynamics were studied in 23 patients with coronary artery disease. After indomethacin administration the systemic arterial pressure increased by 12 +/- 4% and the myocardial oxygen consumption by 24 +/- 11%. Coronary sinus flow did not change and coronary vascular resistance increased slightly. Oxygen saturation of the arterial blood did not change, but coronary sinus saturation decreased substantially. Hemodynamic values returned to normal 150 minutes after administration of indomethacin. During rapid atrial pacing, coronary sinus flow increased 79 +/- 14% above the rest value when pacing was done before indomethacin administration; only a 56 +/- 12% increase was seen when pacing was repeated after indomethacin. Peak heart rate achieved during atrial pacing, severity of angina and the degree of ST-segment depression were not altered by indomethacin treatment. Orally administered indomethacin has a mild coronary vasoconstrictive effect that does not interfere substantially with the expected increase in myocardial blood flow during rapid atrial pacing. Anginal threshold is not altered by orally administered indomethacin.
Administration, Oral↗
Intravenous streptokinase in acute myocardial infarction: experience of community hospitals served by paramedics.
UNLABELLED: We studied 58 consecutive patients, ages 37 to 78, who were given intravenous streptokinase (IV STK) early in the course of acute myocardial infarction (AMI) in three community hospitals served by the same mobile intensive care system. Forty-four patients (76%) received IV STK within 3 hours and 53 patients (92%) received it within 4 hours of onset of chest pain. Half the patients were brought to the hospital by paramedics. The average time from pain to administration of IV STK for paramedic patients was 100 minutes vs 198 minutes for those brought by other modes. Fifty of 58 patients (86%) showed clinical evidence of reperfusion. Forty-six of 54 patients (85%) studied with coronary angiography an average of 6 days post infarction had patent vessels subtending the infarcted region of the myocardium. The average angiographic ejection fraction was 47% for patients with reperfused vessels vs 34% for those with occluded vessels. The in-hospital mortality was 2 of 58 patients (3.4%). There was one late death at 8 months (total 5.2%). Twenty-one patients eventually had coronary bypass surgery and 5 patients had angioplasty. The remaining 29 patients had conventional therapy including 6 months of warfarin sodium. Fifty-four of 55 surviving patients (98%) are in functional class I or II and none have angina at 2 to 18 months of follow-up. Fifty-one of 55 patients are back at work. CONCLUSIONS: (1) IV STK is effective in coronary thrombolysis in a high percentage of AMI patients. (2) IV STK is safely administered in community hospitals.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The usefulness of dobutamine in the assessment of the severity of mitral stenosis.
Patients with mitral stenosis often require supine exercise in order to increase their heart rate and cardiac output to assess the severity of their valvular obstruction during cardiac catheterization. We substituted dobutamine for exercise in 14 patients with suspected mitral stenosis. The dobutamine infusion was started at 5 micrograms/kg/min and was increased to 10, 15, and 20 micrograms/kg/min every 3 minutes as tolerated. The heart rate increased from 84 +/- 4 to 123 +/- 7 bpm (p less than 0.001), the cardiac index increased from 2.4 +/- 0.2 to 3.4 +/- 0.2 L/min/m2 (p less than 0.001), and the mean pulmonary artery pressure increased from 27 +/- 3 to 30 +/- 2 mm Hg (p less than 0.02). The pulmonary wedge pressure of 19 +/- 2 mm Hg and the mitral valve index of 0.8 +/- 0.1 cm2/m2 remained unchanged, but the left ventricular end-diastolic pressure decreased from 11 +/- 2 to 6 +/- 2 mm Hg (p less than 0.02). The hemodynamic response during the infusion of dobutamine identified a subgroup of patients with more severe mitral stenosis. Thus, the administration of dobutamine is useful in the evaluation of the severity of mitral valve obstruction during catheterization.
Adult↗
The response of patients with complex ventricular arrhythmias secondary to dilated cardiomyopathy to programmed electrical stimulation.
A prospective study was undertaken to assess the response of patients with idiopathic dilated cardiomyopathy to programmed electrical stimulation (PES). Fifteen patients undergoing evaluation of congestive heart failure were studied. All patients underwent cardiac catheterization and coronary angiography as well as endomyocardial biopsy to exclude known causes of heart failure. No patient had a history of syncope or sustained ventricular arrhythmias. All patients were found to have severe left ventricular dysfunction (mean ejection fraction 17%), as well as nonsustained ventricular tachycardia on ambulatory monitoring or exercise testing. A protocol using up to two premature stimuli and burst pacing, from two right ventricular sites, induced up to four repetitive ventricular responses but failed to induce a sustained ventricular arrhythmia in any patient. Patients with dilated cardiomyopathy, advanced ventricular arrhythmias, and depressed left ventricular function respond differently than do patients with coronary artery disease, advanced ventricular arrhythmias, and depressed left ventricular function, to PES. PES appears to have limited value in the evaluation of patients with dilated cardiomyopathy and nonsustained ventricular arrhythmias.
Adult↗
Deleterious effects of bretylium on hemodynamic recovery from ventricular fibrillation.
To study the effects of bretylium on the restoration of circulatory function after resuscitation from ventricular fibrillation, closed-chest anesthetized dogs were electrically fibrillated for 1 minute followed by defibrillation (direct-current shock). After one control episode of fibrillation and defibrillation, 16 dogs received a bolus of bretylium (10 mg/kg intravenously). A second episode of fibrillation and defibrillation was induced in eight dogs 3 minutes after bretylium and in eight dogs 4 hours after bretylium. Prior to bretylium, mean arterial blood pressure spontaneously recovered to exceed 200 mm Hg by 2 minutes after defibrillation in all 16 dogs. However, after bretylium, 13 of 16 dogs were in electromechanical dissociation 2 minutes after defibrillation (p less than 0.001). Despite external chest compression, epinephrine, and sodium bicarbonate, a stable blood pressure could not be restored in 6 of 16 dogs. Clofilium, a bretylium analogue lacking sympathetic influences, did not alter the pattern of hemodynamic recovery following defibrillation in five of five dogs. The results suggest that the effects of bretylium on the sympathetic nervous system may profoundly influence the outcome of cardiac resuscitation from fibrillation.
Animals↗
Peripartum cardiomyopathy: clinical, hemodynamic, histologic and prognostic characteristics.
Peripartum cardiomyopathy is defined as left ventricular dilation and failure, first developing during the third trimester of pregnancy or in the first 6 months postpartum. In an effort to characterize this syndrome in a middle class population, 14 consecutive patients with peripartum cardiomyopathy underwent a detailed history and physical examination, right heart catheterization, M-mode and two-dimensional echocardiography, radionuclide ventriculography and right ventricular endomyocardial biopsy. These patients were then observed with sequential noninvasive studies to determine prognostic indicators. Eight (57%) of these 14 patients were primiparous and an equal number first presented with heart failure concomitant with or immediately before the onset of labor. When these women were compared with 55 patients with idiopathic dilated cardiomyopathy, only mean age at onset of symptoms (28.7 +/- 5.7 versus 48.2 +/- 13.6 years, p less than 0.001) and symptom duration (4.1 +/- 7.7 versus 19.0 +/- 18.4 months, p less than 0.001) differed between the groups. There was no difference in ventricular arrhythmia, left ventricular chamber size, ejection fraction or hemodynamics. Myocyte histologic findings were similar; however, myocarditis was identified in 29% of patients with peripartum cardiomyopathy and in only 9% of those with idiopathic dilated cardiomyopathy. In all patients with peripartum cardiomyopathy and myocarditis, the myocardial biopsy was performed within 1 week of onset of symptoms. Seven (50%) of the patients with peripartum cardiomyopathy had dramatic improvement within 6 weeks of follow-up, and 6 (43%) died.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Streptococcus MG-intermedius endocarditis.
Subspeciation of penicillin susceptible alpha-hemolytic streptococci is not routinely performed. However, Streptococcus MG-intermedius is an extremely virulent organism in this strep subgroup and is associated with abscess formation. Our patient, who had endocarditis due to this organism, remained chronically ill despite appropriate antibiotic therapy, and had a perforated aneurysm of the sinus of Valsalva with a myocardial abscess that required extensive surgical debridement. Persistent fever in patients with S MG-intermedius endocarditis should warrant further work-up for metastatic or myocardial abscess formation.
Endocarditis, Bacterial↗
Augmentation of cardiac output by external cardiac pacing: pacemaker-induced CPR.
Transthoracic cardiac pacing is frequently associated with simultaneous stimulation of skeletal muscle and nerves. We describe a patient in cardiogenic shock and complete heart block in whom the associated vigorous abdominal and chest muscle contractions caused by transthoracic cardiac pacing resulted in a marked augmentation of cardiac output and systemic blood pressure via a "CPR" effect.
Aged↗
Sustained postischemic cardiodepression following magnesium-diltiazem cardioplegia.
Magnesium-diltiazem cardioplegia was evaluated in the intact, perfused rat heart to determine whether the joint administration of these agents would adversely affect myocardial contractile and high-energy phosphate recovery following intermittent, normothermic global ischemic arrest. Sequential metabolic and functional analyses were performed on isolated perfused rat hearts during each phase of the experimental protocol: control (10 min), normoxic cardioplegia (10 min), intermittent global ischemic arrest (two 15-min periods separated by 2 min infusion of the normoxic cardioplegic perfusate), and normoxic postischemic control reperfusion (60 min). Four different cardioplegic solutions were evaluated: 30 mM KCl, 30 mM KCl with 2 mg diltiazem/liter, 20 mM MgCl2, and 20 mM MgCl2 with 2 mg diltiazem/liter. Myocardial phosphatic metabolite levels and intracellular pH were analyzed nondestructively in the intact hearts by phosphorus-31 NMR spectroscopy. Corresponding measurements of peak left intraventricular pressure, rate of peak pressure development (dP/dt), and contraction frequency were performed at the midpoint during each 5-min interval of 31P NMR signal averaging. Magnesium plus diltiazem-treated hearts were distinguished from all other groups by a marked delay in postischemic functional recovery consisting of a prolonged depression in contractility (34% of control, P less than 0.01) that persisted throughout the first 50 min of postischemic reperfusion. Diltiazem in combination with magnesium cardioplegia was detrimental to postischemic functional recovery, despite a rapid restoration of high-energy phosphate stores. The apparent adverse interactive effects of excess magnesium and diltiazem suggest that elective ischemic arrest with magnesium cardioplegia in combination with diltiazem may be contraindicated clinically. The mechanistic basis and drug specificity of this response require further clarification. The present findings appear to exclude ATP and PCr production, and structural causes as the basis for the observed aberrant functional recovery from global ischemia of magnesium plus diltiazem-arrested hearts.
Adenosine Triphosphate↗
Pacemaker malfunction: fact or artifact?
In summary, the present examples illustrate how pacemaker malfunction can be simulated by the sources of artifact produced or detected by the monitoring equipment. This form of pseudopacemaker malfunction remains a common cause of mistaken diagnosis of pacemaker malfunction. A thorough understanding of the examples outlined above should help distinguish true pacemaker malfunction from pseudopacemaker malfunction produced by artifact.
Amplifiers, Electronic↗