Surgical management of ventricular tachycardia in subannular left ventricular aneurysm.

Submitral left ventricular aneurysms typically affect young adults of African ancestry. These aneurysms are characterized by heart failure and mitral insufficiency, and occur in the absence of coronary disease. We report a rare case of symptomatic ventricular tachycardia in association with submitral left ventricular aneurysm (and no mitral insufficiency). Ventricular tachycardia was abolished by aneurysm resection and ventricular reconstruction. We suggest surgical management is indicated for ventricular tachycardia associated with this unusual condition, and may be curative.

Septic pulmonary emboli complicating mastoiditis: Lemierre's syndrome revisited.

Deep neck-space infections may cause potentially life-threatening complications of head and neck infections. Lateral pharyngeal space infections in particular predispose to development of suppurative jugular vein thrombosis, which may be associated with anaerobic bacteremia and septic pulmonary emboli (Lemierre's syndrome). We describe a case of Lemierre's syndrome, a very rare entity in the antibiotic era, complicating mastoiditis. Surgical debridement and drainage in conjunction with antibiotic therapy resulted in prompt improvement in the patient's condition.

Tissue characterization of an unusual right atrial mass by magnetic resonance imaging.

In a 70-year-old man who had angina, exercise-induced ventricular tachycardia, and presyncopal symptoms, transthoracic and transesophageal echocardiography disclosed a large atrial mass that resembled a myxoma. Subsequent evaluation by magnetic resonance imaging identified the mass as an intracardiac lipoma attached to the posterior wall of the right atrium, a diagnosis that was confirmed by surgical intervention. Thus, the diagnostic utility of magnetic resonance imaging as an adjunct to echocardiographic evaluation of intracardiac masses was demonstrated.

Surgical management of pericardial diseases.

The institutional experience of the Mayo Clinic in the surgical management of pericardial disease is reviewed. The historical background, indications for, and results of surgical therapy are presented in the management of constrictive pericarditis, effusive pericardial diseases, and recurrent (relapsing) acute pericarditis. With current operative techniques and perioperative management, the vast majority of patients with these conditions can be operated on safely and expect long-term relief of symptoms, with improvement in functional class and survival.

Results of homograft aortic valve replacement for active endocarditis.

Since July 1985, cryopreserved homograft prostheses have been used for aortic valve replacement in 10 patients, aged 2 to 77 years, with active endocarditis. Five patients had positive bacterial cultures from excised valves, and all had clinical findings of uncontrolled infection while receiving appropriate antibiotics. Homograft valves (four) or valved conduits (six) were implanted for treatment of sepsis (6 patients), congestive heart failure (3) or recurrent emboli (1 patient), and complicating native (5 patients) or prosthetic valve (5) endocarditis. Staphylococci (6 patients), streptococci (3), and Candida (1) were infecting organisms. Preoperatively, Doppler echocardiography showed aortic regurgitation in all patients. At operation, 9 patients had gross vegetations, 9 had single or multiple abscess cavities, and 5 had pericarditis. Complex reconstruction of the aortic valve and annulus with homograft conduits was necessary in 6 patients (3 with previous aortoventriculoplasty). Two early deaths (ventricular failure, perioperative stroke) occurred. Mean follow-up of all operative survivors was 2.1 years (range, 0.6 to 3.6 years), and one late death resulted from arrhythmia. Homograft valve regurgitation increased in 1 patient, and 7 late survivors are asymptomatic. No patient has had recurrence of endocarditis. We conclude that cryopreserved homograft aortic valve/root replacement is an effective method for management of active endocarditis complicated by annular destruction.

Electrophysiological effects of left ventricular free wall traction in intact hearts.

Transmural multipolar electrodes, sonomicrometers implanted within the left ventricular wall, and cardiac electrical stimulation techniques were used to examine the effect of transient mechanically applied traction to the left ventricular free wall on local electrophysiological properties. Twenty-five open-chest dogs were atrially paced (cycle length 400 ms) followed by insertion of timed premature extrastimuli at left ventricular epicardial pacing sites either in the vicinity of (traction zone) or remote from (nontraction-control zone) the site of left ventricular free wall traction. Electrophysiological recordings were made before and during intermittent left ventricular free wall traction applied in late diastole (rate 25 cm/s; duration 170 ms). In 22 of 25 dogs, application of traction resulted in early local ventricular activation (mean activation advancement 64 +/- 15 ms), altered QRS morphology of the last conducted atrial drive train beat, and a relative prolongation of ventricular refractoriness in the traction zone. Conversely, in the nontraction-control zone, early activation did not occur and refractoriness was unchanged. Alterations in regional myocardial blood flow (assessed by microsphere technique) did not appear responsible for the observed changes. Furthermore, phenol interruption of local sympathetic or combined sympathetic and parasympathetic innervation or verapamil pretreatment had no impact on the mechanically induced electrophysiological changes. Thus, in normal myocardium in situ, regional abnormalities in wall motion may be associated with alterations of local ventricular activation and refractoriness, factors that in the diseased heart could lead to increased susceptibility to arrhythmias.

Cardiac electrophysiologic effects of orally administered DPI 201-106 in conscious canines: effects of pharmacologic autonomic blockade or cardiac transplantation.

This study assessed the cardiac electrophysiologic effects of DPI 201-106 (DPI), a novel orally absorbable positive inotropic agent, the administration of which has been associated with electrocardiographic (ECG) QT and T-wave changes. In the intact conscious dog, oral administration of both 8 and 16 mg/kg DPI produced marked sinus cycle length prolongation (8 mg/kg, + 11%; 16 mg/kg, + 9%) within 60 min of DPI administration (p less than 0.05 vs. baseline). DPI also tended to prolong right atrial refractory periods, and increase sinus node recovery time. In addition, DPI exhibited a negative dromotropic effect on the atrioventricular (AV) node, prolonging both AV node effective and functional refractory periods and tending to increase the minimum atrial paced cycle length at which AV conduction of 1:1 was maintained. DPI also significantly increased right ventricular effective refractory period (ERP) at both doses studied and increased ventricular functional refractory period (FRP) at the 16-mg/kg dose. Finally, although DPI administration was associated with QT interval prolongation, this effect was slight when corrected for sinus cycle length (SCL) (QTc, +3%). When administered concomitantly with propranolol and atropine or after surgical cardiac denervation, DPI-induced electrophysiologic changes were largely attenuated or abolished. Thus, findings in this study indicate that the apparent cardiac electrophysiologic effects of DPI are predominantly of neurally mediated origin in this animal model.

Acute angular origin of left coronary artery from aorta: an unusual cause of left ventricular failure in infancy.

An unusual congenital anomaly of the left coronary artery, consisting of ostial stenosis caused by an acute angular origin of the vessel from the aorta in an infant, is presented. This anomaly resulted in progressive myocardial fibrosis and development of left ventricular congestive heart failure. The clinical state mimicked anomalous origin of the left coronary artery from the pulmonary artery.

Activities of fluconazole (UK 49,858) and ketoconazole against ketoconazole-susceptible and -resistant Candida albicans.

We have compared the activities of fluconazole and ketoconazole against ketoconazole-susceptible and -resistant strains of Candida albicans in a neutropenic-site rabbit model. Oral treatment with fluconazole resulted in much higher serum and extravascular concentrations of this antifungal agent than did comparable doses of ketoconazole. Fluconazole had no additional in vivo activity against the ketoconazole-susceptible strains; no fungicidal activity was observed with peak drug levels as high as approximately 75 micrograms/ml in the infection sites. Significant fungistatic activity against the ketoconazole-resistant strains was observed with fluconazole treatment (80 mg/kg), but not with less fluconazole (20 mg/kg) or with ketoconazole (approximately 67 mg/kg). In vitro susceptibility tests separated the ketoconazole-susceptible strains from the ketoconazole-resistant strains, but the results were variable when the resistant strains were tested with fluconazole.

The effects of verapamil on left ventricular function in the presence of beta-adrenergic blockade.

Supraventricular tachyarrhythmias frequently complicate myocardial revascularization. Intravenous administration of verapamil has been effective in terminating these arrhythmias. To determine the effects of verapamil on left ventricular systolic function, we implanted ultrasonic dimension transducers in dogs and, after they had recovered from the operation, studied them while they were awake and unsedated. Intravenous administration of verapamil (0.2 mg/kg) resulted in an elevation of cardiac output above baseline because of reflex-induced tachycardia. Contractility, as measured by the load-independent end-systolic pressure-volume relationship, remained unchanged. When the animals were pretreated with atropine and propranolol, verapamil resulted in a fall in cardiac output and contractility. The intact animal responded to the vasodilatory effect of verapamil by releasing catecholamines to maintain cardiac output and hemodynamic stability. Only when this compensatory mechanism was blocked by a beta-adrenergic blocker do the inherently negative inotropic and chronotropic effects of verapamil become apparent. The clinical ramifications of this finding are of greater importance to the surgeon as more patients receive beta-adrenergic blocking agents up to the time of the immediate preoperative period. We conclude that verapamil should be administered with caution to patients with supraventricular tachyarrhythmias who have been receiving beta-adrenergic blocking agents.

Effects of transplantation on atrioventricular nodal accommodation and hysteresis.

In the present study, atrioventricular nodal accommodation and hysteresis characteristics were evaluated in awake, unsedated dogs, before (n = 10) and after cardiac transplantation (n = 10). Chronically instrumented animals were atrially paced at a cycle length (CL) of 400 ms, followed by an abrupt decrease in pacing CL to 300 ms, followed by an abrupt return in pacing CL to 400 ms (with pacing sustained for 60 s at each CL). Atrioventricular nodal conduction characteristics (assessed by AH intervals) were simultaneously monitored. Under control conditions, AH intervals lengthened rapidly after an abrupt decrease in pacing CL [mean time for AH interval lengthening to stabilize (Tonset) = 2 +/- 1 s], whereas AH intervals lengthened more slowly (P less than 0.05) after transplantation (Tonset = 41 +/- 4 s). Similarly, after an abrupt increase in pacing CL, control AH intervals shortened rapidly [mean time for AH interval to return to base line (Tonset) = 5 +/- 1 s], whereas AH intervals shortened more slowly (P less than 0.05) after transplantation (Tonset = 42 +/- 5 s). Thus accommodation appears to be an intrinsic atrioventricular nodal response (present after cardiac denervation by transplantation) to abrupt, sustained atrial CL changes. Furthermore equivalence (P = NS) in atrioventricular nodal accommodation responses to symmetric CL decreases and increases after transplantation suggests that hysteresis [i.e., nonequivalence (P less than 0.05) in atrioventricular nodal accommodation responses], as seen under control conditions, results primarily from extrinsic (neural) modification of intrinsic atrioventricular nodal responses to symmetric CL changes.

Left ventricular dysfunction in a canine model of chronic cyanosis.

States of low cardiac output frequently complicate the postoperative course of patients undergoing repair of cyanotic congenital heart lesions. The relative contribution of chronic cyanosis alone to the postoperative deterioration in left ventricular function remains unknown. To study the effects of chronic cyanosis on left ventricular function, nine dogs underwent inferior vena cava-to-left atrial anastomosis, a model that minimizes abnormal left ventricular hemodynamic loads. After at least 6 months of chronic cyanosis (mean arterial pO2 of 44 mm Hg and mean hematocrit of 61%), the dogs were instrumented with ultrasonic dimension transducers and micromanometers for collection of left ventricular pressure-dimension data. Studies were performed 7 to 10 days after recovery from instrumentation while the dogs were awake and alert. Nine normal dogs were also instrumented and served as controls. Pressure and dimension data were collected during transient vena cava occlusions before and after the combined administration of propranolol and atropine to produce autonomic blockade. Contractile function as measured by dP/dt, ejection fraction, and the stroke work-end diastolic length relationship was decreased by autonomic blockade to a similar extent in both normal and cyanotic dogs. After autonomic blockade, normal dogs were able to maintain stroke volume and cardiac index by utilization of Frank-Starling reserves (increased left ventricular end diastolic volume). In contrast, dogs with cyanosis were unable to maintain stroke volume and cardiac index or to increase left ventricular end diastolic volume after autonomic blockade. Dogs with cyanosis had reduced ventricular diastolic compliance, and they more fully used Frank-Starling reserves to maintain normal stroke volume and cardiac index in the control state when compared with normal dogs. The diminished preload reserves of the cyanotic dogs limited systolic performance (stroke volume and cardiac index) only at reduced levels of contractility produced by autonomic blockade.

Potentiation of cardiac electrophysiologic effects of verapamil after autonomic blockade or cardiac transplantation.

Cardiac electrophysiologic effects of verapamil in vivo are the result of both direct and indirect actions on the heart (the latter due to augmentation of sympathetic neural tone, diminution of parasympathetic neural tone, and increased circulating catecholamines). In this study we assessed the interaction of verapamil's direct and indirect actions on electrophysiologic properties of the heart in awake, previously instrumented, unsedated dogs. After administration of intravenous verapamil (0.2 mg/kg), electrophysiologic effects were assessed serially over a 1 hr period in 10 awake dogs before (group 1 studies) and during pharmacologic autonomic blockade (group 2 studies), and in a subset of these dogs (n = 5) after orthotopic cardiac transplantation (group 3 studies). In group 1 dogs, sinus cycle length (SCL) initially shortened after verapamil (postverapamil 379 +/- 50 msec vs baseline of 494 +/- 72 msec, p less than .001) and subsequently gradually prolonged. In groups 2 and 3, transient SCL shortening was absent. SCL prolonged promptly after verapamil, and sinus arrest developed in two of 10 group 2 and two of five group 3 animals. Verapamil exerted a negative dromotropic effect on atrioventricular node conduction in all three experimental groups, as assessed by drug-induced changes in minimum cycle length with sustained 1:1 atrioventricular conduction and measurements of atrioventricular node effective and functional refractory period. However, compared with findings in group 1, this negative dromotropic effect occurred more rapidly and was markedly potentiated in groups 2 and 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic effects of papillary muscle traction in the intact heart.

In this study we used transmural multipolar electrodes, sonomicrometers implanted within the left ventricular wall, and cardiac electrical stimulation techniques to examine the effect of transient mechanical posterior papillary muscle traction on local myocardial electrophysiologic characteristics. Nine open-chest dogs were atrially paced (cycle length 400 msec) followed by insertion of timed premature extrastimuli at left ventricular epicardial pacing sites either in the vicinity of (traction zone) or remote from (nontraction zone) the site of papillary muscle traction. Electrophysiologic recordings were made before and during periods of intermittent papillary muscle traction of predetermined timing, application rate (25 cm/sec), and duration (170 msec). Papillary muscle traction was applied in late diastole just before the last beat of each atrial drive train. In seven of nine dogs application of transient papillary muscle traction resulted in significantly earlier local ventricular activation (mean activation advancement 30 +/- 13 msec), altered QRS morphology of the last conducted atrial drive-train beat, and relative prolongation of ventricular functional refractory period in the traction zone. Conversely, in nontraction zones in these seven dogs, early activation did not occur and refractoriness remained unchanged as tested by a locally placed extrastimulus. In two of nine dogs traction failed to induce early activation and changes in refractoriness did not occur. Alterations in regional myocardial blood flow (assessed by radioactive microsphere technique) did not appear responsible for the observed changes, since there was no demonstrable traction-induced difference in regional blood flow between the traction and nontraction zones.(ABSTRACT TRUNCATED AT 250 WORDS)

Kinetics of electrophysiologic changes during oral loading of amiodarone and after withdrawal of amiodarone in the unsedated dog.

We examined the temporal kinetics of onset and offset of the cardiac electrophysiologic effects of orally administered amiodarone in chronically instrumented, unsedated adult dogs (n = 8). Right atrial (RA), atrioventricular nodal (AVN), and right ventricular (RV) effective refractory period (ERP), and AVN functional refractory period (FRP), were determined daily for 21 days during amiodarone loading (24 mg/kg/day) and for 21 days after cessation of amiodarone. Left ventricular (LV) ERP was assessed in four of eight animals. Group mean RA-ERP peaked and plateaued early during amiodarone loading (time to reach one-half observed peak change [t1/2 onset] = 1.2 +/- 0.5 days) and rapidly returned toward baseline after cessation of drug (decay time to one-half peak value [t1/2 offset] = 2.0 +/- 1.7 days). Group mean RV-ERP rose in a linear manner throughout the loading period (t1/2 onset = 9.3 +/- 2.1 days) and remained elevated after cessation of drug (t1/2 offset greater than 21.0 days). Group mean AVN-ERP and FRP exhibited temporal kinetics intermediate between those of the RA-ERP and RV-ERP, both during amiodarone loading and after cessation of the drug. Group mean LV-ERP onset kinetics (assessed in a limited number of animals, n = 4) appeared to differ from RV-ERP onset kinetics (t1/2 onset = 2.5 +/- 2.5 days), whereas LV-ERP and RV-ERP offset kinetics appeared similar (t1/2 offset greater than 21 days). In summary, our findings demonstrate that during oral loading, the temporal sequence of onset of amiodarone-induced electrophysiologic effects is site dependent. Similarly, after cessation of amiodarone, the persistence of drug-induced electrophysiologic effects is both variable and site dependent.