Elevated arginine vasopressin and lowered atrial natriuretic factor associated with hypertension in coarctation of the aorta.

Impairment of humoral and neural regulation of blood pressure may contribute to preoperative and postoperative hypertension in coarctation of the aorta and may also affect the release of vasopressin and atrial natriuretic factor. Because vasopressin and atrial natriuretic factor have potent vasoactive effects, we measured plasma vasopressin and atrial natriuretic factor levels by radioimmunoassay before operation and for 5 days after operation in 11 patients aged 9 months to 12 years undergoing coarctation repair and in 12 control patients undergoing other cardiovascular operations. Six patients in the coarctation group required minimal antihypertensive therapy (group I) and five required prolonged intravenous antihypertensive therapy (group II). Before operation, vasopressin levels correlated with systolic blood pressure for all patients in the coarctation group (r = 0.83, p < 0.01) whereas atrial natriuretic factor levels did not. Before operation, atrial natriuretic factor levels were lower (28 +/- 5 vs 41 +/- 7 and 50 +/- 8 pg/ml, p < 0.05) and vasopressin levels were higher (28 +/- 6 vs 5.4 +/- 0.9 and 7 +/- 3 pg/ml, p < 0.05) in group II than in group I or control patients. Vasopressin levels were higher (p < 0.05) on the day of operation and on postoperative days 2 through 5 in group II than in group I and in control patients. Atrial natriuretic factor levels were lower during the day of operation in group II than in group I or in control patients (26 +/- 7 vs 51 +/- 16 and 50 +/- 7 pg/ml, p < 0.05) and remained lower than control values on postoperative days 1 and 3 through 5. Elevated vasopressin and lowered atrial natriuretic factor levels may contribute to preoperative and postoperative hypertension in coarctation.

Congenital anomalies of the coronary arteries. Classification and significance.

An understanding of the anomalies of the coronary arteries is imperative for physicians dealing with diagnosis and treatment of coronary artery disease. Although not as common as acquired coronary artery disease, congenital coronary anomalies contribute to significant morbidity and mortality. In addition, they may present difficulties for the angiographer at the time of catheterization, as well as a challenge for the radiologist in interpretation. To facilitate a better understanding of these anomalies, a new classification is presented, together with illustrations and discussion of the clinical significance.

Noncardiac chest pain in adolescents and children with mitral valve prolapse.

Chest pain in adolescents and children is usually not of cardiac origin. Of cardiac conditions commonly linked to chest pain in childhood, mitral valve prolapse (MVP) is the most prevalent, but this association has recently been questioned. In light of recent reports of gastroesophageal sources of chest pain in adults with MVP, we performed a comprehensive gastroesophageal evaluation of 17 preadolescents and adolescents with mitral valve prolapse who had chest pain as their presenting symptom. Evaluation consisted of esophageal manometry, Bernstein test, esophageal pH probe, and/or esophagogastroscopy. Fourteen of the 17 patients had at least one abnormal finding. Five patients had esophagitis, five had gastritis, one had high-amplitude esophageal contractions, one had abnormal esophageal manometry with positive Bernstein test, one had esophageal reflux and positive Bernstein test, and one had abnormal manometry with esophageal reflux. The 13 patients with esophagitis, gastritis, reflux, or positive Bernstein test were treated with antacid, with resolution of chest pain in 12 patients. Two of these patients underwent follow-up endoscopy with documentation of improvement. The patient with high-amplitude esophageal contractions was treated with dicyclomine, which resulted in resolution of chest pain. The observation that the chest pain was not related to mitral valve prolapse is important in clinical practice and raises further questions as to whether mitral valve prolapse causes chest pain.

Recognition of bicuspid aortic valve by plain film calcification.

Differentiation of bicuspid aortic valve from other causes of calcific aortic stenosis is not possible by echocardiography or, in many cases, by aortography. This report describes newly recognized patterns of calcification on plain films that are diagnostic for a bicuspid aortic valve. These are based on identification of the calcified raphe and/or the calcified conjoint leaflet. In 120 patients who underwent surgical repair of calcific aortic stenosis, 40 were found to have bicuspid valve. Examination of the plain films retrospectively allowed a correct recognition of 26 (65%) of these valves. In contrast, only 10 (25%) could be recognized by aortography. Patterns of calcification on plain films represent an important tool for detection of calcified cogenital bicuspid aortic valve.

Umbilical artery catheters and blood flow velocities in the superior mesenteric artery: effect of insertion, removal, aspiration, and bolus infusion.

PURPOSE: We studied whether umbilical artery catheters (UACs) affect blood flow in the superior mesenteric artery (SMA) of neonates. METHODS: Noninvasive duplex pulsed Doppler sonography was used to measure peak systolic velocity, end-diastolic velocity, and mean flow velocity in the SMA. The resistance index and pulsatility index were calculated from these data. Thirty-two infants weighing 450-2,520 g at birth were enrolled in the study. Gestational age at birth was 24-37 weeks. Eighteen infants were studied before and after UAC insertion. Twenty infants were studied before and after UAC removal. Eleven infants with UACs were studied before and during aspiration of blood from the UAC and during bolus infusion of 5% dextrose solution into the UAC. Data were compared before and after UAC insertion; before and after UAC removal; and before and during aspiration and during bolus infusion. RESULTS: Blood flow velocities and vascular resistance were similar in all comparisons except for increases in end-diastolic and mean velocities after UAC insertion. CONCLUSIONS: Insertion and removal of UACs, aspiration of blood from UACs, and bolus infusion of fluids into UACs do not diminish blood flow velocity or increase vascular resistance in the SMA.