Supraventricular Tachycardia Induced by Swallowing: A Case Report and Review of the Literature

A 64-year-old man who complained of palpitations brought on by swallowing was found to have short runs of paroxysmal supraventricular tachycardia (SVT) induced by swallowing. Electrophysiology studies suggested that the SVT was an automatic atrial tachycardia. An esophageal manometric study demonstrated that the tachycardia was coincident with relaxation of the upper esophageal spincter and preceded peristaltic activity in the esophageal body. Atropine and bethanechol did not affect the swallow-induced tachycardia. The patient's symptoms were controlled by verapamil and quinidine. After five months, these medications were discontinued, with no recurrence of symptoms. Based on analysis of ten prior cases and the present case, it appears that swallow-induced SVT generally occurs in men between the ages of 45–75 years who have no evidence of structural heart disease or an esophageal disorder. The SVT is usually either a nonsustained automatic atrial tachycardia or atrial fibrillation. The mechanism is conjectural, but the most likely possibility is a vagally-mediated neural reflex, probably involving a neu-rotransmitter other than acetylcholine.     

Device Use Patterns and Clinical Outcome of Implantable Cardioverter Defibrillator Patients with Moderate and Severe Impairment of Left Ventricular Function

The beneficial effects of implanted cardioverter defibrillator (ICD) therapy in patients with malignant ventricular tachyarrhythmias and variable degrees of left ventricular (LV) dysfunction are debated. ICD use and patient survival were examined in 128 patients with malignant ventricular arrhythmias and moderate or severe LV dys function. Group I included 64 patients with moderate LV dysfunction (LV ejection fraction of > 30%) and group H, 64 patients with severe LV dysfunction (LV ejection fracfion of ≤ 30%). Follow-up period ranged from 1 to 78 months. The two groups were similar in age, incidence of coronary artery disease and presenting arrhythmia. The mean LV ejection fraction in group I was 44%± 8% and group II was 22%± 5% (P < 0.0001). At 4 years of follow-up, 66% of patients from group I and 62% from group II (P = NS) had ICD activation for presumed ventricular tachyarrhythmia. Survival was calculated using actuarial analysis. Arrhythmic or sudden death mortality at 4 years of follow-up was 4% in group I and 7% in group II (P = NS). Cardiac mortality was for group I, 7% (P < 0.05), 12% (fP < 0,01), 15% (P < 0.01), and 15% (P < 0.01) for follow-up years 1, 2, 3, and 4, respectively. For group II, cardiac mortality was 27%, 36%, 41%, and 41% for follow-up years for 1, 2, 3, and 4, respectively. The majority of cardiac deaths in both groups was observed in the first 2 years of follow-up. However, in both groups, cardiac mortality was comparable in patients who did (users) and did not (nonusers) experience appropriate ICD shocks. Thus, the incidence of long-term ICD use is comparable in patients with moderate and severe LV dysfunction. Cardiac mortality is higher in patients with severe LV dysfunction in the first 4 years of follow-up irrespective of device use. The comparable long-term clinical outcome of ICD users and non users in patients with moderate or severe LV dysfunction can be related to elimination of arrhythmic mortality. Long-term patient survival in ICD recipients with severe LV dysfunction remains substantial even at 4 years of follow-up.     

Conversion of exogenous arachidonic acid to prostaglandins in the pulmonary circulation in vivo A human and animal study

The capacity of human lungs to synthetize prostaglandins (PGs) from exogenous arachidonic acid (AA) was investigated in healthy male volunteers. ¹⁴C-labelled AA was infused at a constant rate into the right atrium under simultaneous sampling of blood from the ascending aorta. The arterial content of ¹⁴C-AA metabolites was extracted, separated with thin-layer chromatography and quantified using fractionated liquid scintillation spectrometry. Conversion of exogenous AA to prostacyclin (PGI₂) was also studied in the lungs of anaesthetized cats. In these experiments different doses of unlabelled AA were administered intravenously. Simultaneously PGI₂-activity in the arterial blood was assayed using a technique for continuous measurement of platelet aggregation on blood superfused collagen strip. Radiochromatograms of the human arterial plasma revealed no clearly defined peaks corresponding to any of the unlabelled standards of PGD₂, PGE₂, 6-keto-PGF_1α, PGF_2α or TxB₂. The ¹⁴C-activity in the chromatograms materialized only in one (apart from AA) prominent peak in parallel to 13,14-dihydro-15-keto-PGE₂. Neither in cats did significant amounts of PGI₂ appear in the arterial blood after administration of AA in moderate doses. Only very high AA doses caused a slight increase in arterial PGI₂-activity. The results demonstrate that human lungs do not convert exogenous AA to PGs under physiological conditions. In cats the reluctance of the lungs to utilize exogenous precursor can only be overcome with high, non-physiological AA doses. The data may suggest the existence of special regulatory mechanisms which control release of PGs from the lungs and promote utilization of endogenous precursor.     

Reactive Naphthalene Metabolite Binding to Hemoglobin and Albumin

Earlier work has shown that the murine Clara cell cytotoxi cant,naphthalene, is metabolized to reactive metabolites which depleteglutathione or, in the absence of sufficient glutathione, becomebound covalently to tissue macromolecules. Correlations betweenbound metabolite levels in the lung with injury suggests anassociation between reactive metabolite binding and toxicity.In this study we examine the formation of covalent naphthaleneadducts with hemoglobin and albumin in mice to determine whetherthese serve as useful indices of exposure and metabolism fora chemical which shows a glutathione threshold. Covalent bindingof radioactivity from [³]naphthalene to both albumin and hemoglobinwas dose dependent and a glutathione threshold was observed.At early times after naphthalene administration, the formationof albumin adducts was 10- to 30-fold higher than that of hemoglobinadducts. Hemoglobin and albumin adduct levels decreased by apparentfirst-order processes with half-lives of 11.5 and 1.8 days,respectively. These half-lives are consistent with the turnoverof these blood proteins in the mouse. Pretreatment with buthioninesulfoximine resulted in higher levels of albumin adduct butin no alteration of hemoglobin adduct levels in comparison withcontrol. In contrast, diethylmaleate pretreatment increasedthe level of hemoglobin adduct but not albumin adduct. The antibodyto naphthalene mercapturates recognized the hemoglobin adduct(s)but not the albumin adduct(s). Comparison of the data from ELISA(standardized using hydroxymercaptodihydronaphthalene) and radiochemicalanalysis yielded curves with identical slopes; the absolutelevels of adduct found by ELISA were approximately half thosemeasured with radiochemical techniques. These studies indicatethat high levels of reactive naphthalene metabolites are boundto hemoglobin and albumin at doses above the glutathione threshold.Although hemoglobin adduct levels can be monitored sensitivelywith ELISA, the presence of the glutathione threshold suggeststhat monitoring exposed populations may not provide a usefulmeasure of exposure at environmentally relevant exposure levels.     

Comparison of Clinical Benefits and Outcome in Patients with Programmable and Nonprogrammable Implantable Cardioverter Defibrillators

Technological advances in implantable cardioverter defibrillators (ICDs) have provided a variety of programmable parameters and antitachycardia therapies whose utility and impact on clinical outcome is presently unknown. ICDs have capabilities for cardioversion defibrillation alone (first generation ICDs), or in conjunction with demand ventricular pacing (second generation ICDs), or with demand pacing and antitachycardia pacing (third generation ICDs). We examined the pattern of antitachycardia therapy use and long-term survival in 110 patients with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Group I included 62 patients with nonprogrammable first generation ICDs that delivered committed shock therapy after ventricular tachyarrhythmia detection based on electrogram rate and/or morphology was satisfied. Group II included 48 patients with multiprogrammable ICDs (including second and third generation ICDs) that had programmable tachyarrhythmia detection based on rate and tachycardia confirmation prior to delivery of electrical treatment with either programmable shocks and/or, as in the third generation ICDs, antitachycardia pacing. Incidence and patterns of antitachycardia therapy use and long-term survival were compared in the two groups. The incidence of appropriate shocks in patients who completed 1 year of follow-up was significantly greater in group I (30 of 43 patients = 70% vs 11 of 26 patients = 42%; P less than 0.05). In the total follow-up period, a significantly larger proportion of group I patients as compared to group II patients used the shock therapies (46 of 62 patients = 74% vs 25 of 48 patients = 52%; P less than 0.01), with the majority doing so within the first year of implantation (96% and 92%, respectively). Although the frequency of antitachycardia therapy activation was similar, the number of shocks delivered per patient was lower in group II, particularly in the initial 3 months of follow-up (P = 0.06). No clinical variable aided in identifying users from nonusers of antitachycardia therapy. Arrhythmic mortality was virtually eliminated in both groups. Two-year actuarial cardiac survival in the two groups was similar (group I = 78% vs group II = 84%; P greater than 0.2). Survival from cardiac mortality in users and nonusers of antitachycardia therapies was also similar in both groups (P greater than 0.2) and in the total patient group (P greater than 0.2). We conclude that programmable ICDs continue to confer advantages in prevention of sudden death that were observed with nonprogrammable ICDs and can be expected to improve patient tolerance and physician acceptance of device therapy for VT/VF.