Journal of the American College of Cardiology
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J. Am. Coll. Cardiol. · Aug 1987
Surgical management of subaortic obstruction in single left ventricle and tricuspid atresia.
Subaortic obstruction caused by either a restrictive bulboventricular foramen in single left ventricle with an outflow chamber or by a restrictive ventricular septal defect in tricuspid atresia with transposition of the great arteries can lead to a hypertrophied, noncompliant ventricle and excessive pulmonary blood flow. This combination is disadvantageous to potential Fontan procedure candidates because they are dependent on good ventricular function and low pulmonary vascular resistance for survival. The results of surgical procedures to directly or indirectly relieve significant subaortic obstruction (gradient greater than 30 mm Hg) in 24 patients, 16 with single left ventricle and 8 with tricuspid atresia, were reviewed. ⋯ These data show that: Surgical relief of established subaortic obstruction in patients with single left ventricle and tricuspid atresia carries a high mortality rate, especially if the subaortic gradient is greater than 75 mm Hg. The best procedure appears to be the pulmonary artery to ascending aorta anastomosis. A clearer understanding of the factors leading to the development of significant subaortic obstruction is necessary to prevent it or to devise improved therapeutic strategies.
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J. Am. Coll. Cardiol. · Jun 1987
Double-blind study of intravenous propafenone for paroxysmal supraventricular reentrant tachycardia.
Propafenone was administered during electrophysiologic testing to determine its efficacy and safety for terminating and preventing reinduction of paroxysmal supraventricular reentrant tachycardia. Four men and 10 women (mean age 50 years, range 28 to 69) were studied. Five patients had Wolff-Parkinson-White syndrome with orthodromic atrioventricular (AV) reentrant tachycardia, three had a concealed accessory pathway with AV reentrant tachycardia and six had tachycardia due to reentry within the AV node. ⋯ Of the nine patients receiving long-term oral propafenone therapy, eight had a reduction of at least 90% in reentrant tachycardia during a mean follow-up period of 14.5 months (range 11 to 22); all eight patients had had noninducible reentrant tachycardia after intravenous propafenone. One patient had increased frequency of reentrant tachycardia; this patient had had inducible reentrant tachycardia after intravenous propafenone. In conclusion, intravenously administered propafenone terminated reentrant tachycardia in 85% of patients and prevented reinduction in 71%, with no adverse hemodynamic effects.
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J. Am. Coll. Cardiol. · Jun 1987
Combination of tocainide and quinidine for better tolerance and additive effects in patients with coronary artery disease.
The efficacy and tolerance of tocainide used alone and in combination with quinidine were studied in 20 patients with coronary artery disease and frequent (greater than 30/h) ventricular premature complexes. Holter electrocardiographic monitoring was performed at baseline and during therapy with tocainide alone, quinidine alone and a combination of tocainide and quinidine. During single drug therapy, the dose of tocainide was 1,680 +/- 437 mg/day and that of quinidine was 1,340 +/- 235 mg/day. ⋯ Compared with baseline values (100%), the frequency of ventricular premature complexes was reduced to 33 +/- 44% with quinidine, 39 +/- 30% with tocainide and 10 +/- 16% with combination therapy (p less than 0.01 for combination versus quinidine or tocainide alone; p = NS for quinidine versus tocainide). Individually, an effective regimen (greater than 83% reduction of ventricular premature complexes and abolition of nonsustained ventricular tachycardia) was found in 3 (15%) of 20 patients receiving tocainide alone, in 6 (30%) receiving quinidine alone and in 16 (80%) receiving combination therapy (p less than 0.01 for tocainide versus combination, quinidine versus combination; p = NS for tocainide versus quinidine). Thus, the antiarrhythmic effects of quinidine and tocainide are additive.(ABSTRACT TRUNCATED AT 250 WORDS)
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J. Am. Coll. Cardiol. · Feb 1987
ReviewLouis F. Bishop lecture. Role of coronary artery spasm in symptomatic and silent myocardial ischemia.
The revival of the concept of coronary spasm has stimulated research into coronary artery disease. Observations in patients with variant angina have substantially contributed to the appreciation of painless myocardial ischemia. However, the presence or absence of pain during ischemic episodes is not related to the cause of ischemia, because painless ischemia can be observed in variant angina (caused by spasm), in effort-induced angina (caused by increased myocardial demand) and in myocardial infarction (caused by thrombosis). ⋯ Dynamic stenosis can be caused by 1) "physiologic" increase of coronary tone, as in stable angina, 2) spasm, as in variant angina, and 3) thrombosis, usually in combination with "physiologic" changes in tone or with spasm, or both, as in unstable angina. The mechanisms of spasm, as typically observed in variant angina, are different from those of "physiologic" increase of tone; they appear to be related to a local alteration that makes a segment of coronary artery hyperreactive to a variety of constrictor stimuli causing only minor degrees of constriction in other coronary arteries. The nature of this abnormality, which may remain stable for months and years, is yet unknown.
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J. Am. Coll. Cardiol. · Jan 1987
Case ReportsAtrial septal defect with right to left shunt despite normal pulmonary artery pressure.
A 74 year old woman had right to left shunting through an atrial septal defect despite normal right heart pressures. Acute volume expansion temporarily reduced the shunt. Contrast echocardiography and angiography demonstrated that this shunting occurred almost exclusively from the inferior vena cava. At surgery a redundant flap of septum secundum was found that was adjacent to the inferior vena cava orifice, intercepting its blood return like a spinnaker and shunting it into the left atrium.