[Incidence and severity of coronary artery disease in patients with acute aortic dissection: comparison with abdominal aortic aneurysm and arteriosclerosis obliterans].

OBJECTIVES: The incidence and severity of coronary artery disease were studied in patients with acute aortic dissection (AAD), and compared with coronary artery disease in patients with abdominal aortic aneurysm (AAA) or arteriosclerosis obliterans (ASO). METHODS: A total of 71 patients(42 males, 29 females, mean age 61.4 +/- 10.0 years) with AAD, undergoing coronary angiography between 1988 and 1999, were studied including 38 patients with open communication type and 33 patients with thrombosed type. According to the Stanford classification, 18 patients were type A and 53 patients were type B. Patients with AAD following Marfan syndrome or chest trauma were excluded from the study. Selective coronary angiography was performed in age- and sex-matched patients with AAA(n = 57; 42 males, 15 females, mean age 63.9 +/- 4.6 years) or ASO (n = 95; 66 males, 29 females, mean age 62.4 +/- 9.4 years). Coronary artery disease was defined as > or = 75% stenosis (left main trunk lesion of > or = 50% stenosis) by multidirectional imaging. RESULTS: Significant coronary artery disease was demonstrated in 14 patients with AAD (19.7%), 25 patients with AAA (43.9%), and 49 patients with ASO (51.5%). The incidence of coronary artery disease was significantly lower in the AAD group than in the other two groups (p < 0.05). One-vessel disease was present in approximately 70% of the patients with AAD and coronary artery disease. In contrast, multivessel disease was observed in approximately 50% of patients with AAA and ASO. Classification of the patients with AAD according to the blood flow in the false lumen showed coronary artery disease was more highly associated with the thrombosed type [10 (30.3%) of 33 patients] than the open communication type [4 (10.5%) of 38 patients]. Multivariate logistic regression analysis of the patients with AAD showed coronary artery disease was associated with a high serum total cholesterol level (p = 0.025) and the thrombosed type (p = 0.043). CONCLUSIONS: The incidence of coronary artery disease was significantly lower among patients with AAD than among age- and sex-matched patients with AAA or ASO. Coronary artery disease developed in 30% of the patients with the thrombosed type of AAD, although the prognosis seemed to be good.

ST segment elevation in the right precordial leads following administration of class Ic antiarrhythmic drugs.

Electrocardiographic changes were evaluated retrospectively in five patients without previous episodes of syncope or ventricular fibrillation who developed abnormal ST segment elevation mimicking the Brugada syndrome in leads V1-V3 after the administration of class Ic antiarrhythmic drugs. Pilsicainide (four patients) or flecainide (one patient) were administered orally for the treatment of symptomatic paroxysmal atrial fibrillation or premature atrial contractions. The QRS duration, QTc, and JT intervals on 12 lead surface ECG before administration of these drugs were all within normal range. After administration of the drugs, coved-type ST segment elevation in the right precordial leads was observed with mild QRS prolongation, but there were no apparent changes in JT intervals. No serious arrhythmias were observed during the follow up periods. Since ST segment elevation with mild QRS prolongation was observed with both pilsicainide and flecainide, strong sodium channel blocking effects in the depolarisation may have been the main factors responsible for the ECG changes. As the relation between ST segment elevation and the incidence of serious arrhythmias has not yet been sufficiently clarified, electrocardiographic changes should be closely monitored whenever class Ic drugs are given.

Circadian variation of vasovagal syncope.

INTRODUCTION: Circadian patterns have been demonstrated for several cardiovascular catastrophes. Chronobiologic factors play a role in the emergence of vasovagal syncope (VVS); however, diurnal variation of syncopal episodes in VVS has not been reported previously. METHODS AND RESULTS: We assessed daily distribution of the time of syncopal episodes in VVS. Time of syncope could be determined in 80 episodes in 54 patients (32 men and 22 women; mean age 37 years, range 12 to 67). Patients who were prescribed beta blockers or vasodilators, and who had syncopes related to alcohol intake, were excluded from the study. Head-up tilt testing was performed in 53 patients. The distribution of the episodes of VVS in 3-hour intervals differed significantly from uniform occurrence (P < 0.0001), with a peak frequency between 6 A.M. and noon (67.5% of total episodes). In patients who had experienced the initial syncope in the morning, most (78%) of the next syncopal episodes also occurred in the morning. There was no significant correlation between the time of last syncopes and tilt testing results. CONCLUSION: We demonstrated a prominent circadian variation in the frequency of VVS, with a peak in the morning. Recognition of the daily distribution of VVS is useful for patient education and therapeutic strategy.

[Methodology of 80 degrees head-up tilt testing with and without low dose isoproterenol provocation in Japanese patients with neurally mediated syncope].

The usefulness of 80 degrees head-up tilt testing with and without low dose isoproterenol provocation was evaluated for the diagnosis of neurally mediated syncope (NMS) in Japanese. Head-up tilt testing was performed in 114 consecutive patients with clinical diagnoses of NMS (68 men, 46 women, mean age 46 +/- 21 years), and 57 times in 36 healthy volunteers (26 men, 10 women, mean age 31 +/- 8 years) who had no history of syncope or presyncope. Head-up tilt testing used an 80 degrees angle for 30 minutes (passive tilt), and if the passive tilt resulted in negative response, isoproterenol was infused at 0.01-0.02 microgram/kg/min and the tilt repeated for 10 minutes (isoproterenol tilt). A positive response was defined as the development of syncope or a presyncopal state associated with hypotension, bradycardia or cardiac arrest. The sensitivities of passive tilt testing for a positive response after 5-, 10-, 15-, 20-, 25- and 30-minute tilting were 1%, 9%, 14%, 19%, 24%, and 28%, respectively, and specificities after 5-, 10-, 15-, 20-, 25- and 30-minute tilting were 100%, 95%, 91%, 88%, 86%, and 84%, respectively. The sensitivities of isoproterenol tilt testing with 0.01 and 0.02 microgram/kg/min were increased to 37% and 48%, respectively. This improvement was statistically significant between the passive tilt and isoproterenol tilt testing with a dose of 0.02 microgram/kg/min (p < 0.01). However, specificities were comparable with those of the passive tilt testing (84% and 82%, respectively). In conclusion, 80 degrees passive tilt testing for 30 minutes showed a low sensitivity (28%) but acceptable specificity (84%). Low-dose isoproterenol provocation was useful for improving sensitivity (48%) while maintaining a comparable specificity (82%).

Does an early increase in heart rate during tilting predict the results of passive tilt testing?

Head-up tilt testing is a useful but time-consuming procedure. If we could accurately predict the tilt testing results; we would be able to substantially shorten the duration of tilt protocol. To clarify the hypothesis that an early increase in heart rate (HR) during tilting can predict the passive tilt results in our protocol (80-degree angle for 30 minutes), we studied 115 consecutive patients (72 men, 43 women, mean age 46 +/- 19 years) who were clinically diagnosed with neurally mediated syncope. Twenty-nine (25%) patients had a positive tilt test (P group), whereas 86 (75%) patients had a negative test (N group). The early HR increase was defined as the maximum HR during the first 5 minutes of tilting minus the resting HR before tilting. The early HR increase was significantly higher in the P group (23.8 +/- 9.5 beats/min) than in the N group (17.5 +/- 8.2 beats/min, P = 0.0008), but it was negatively correlated with the tilt duration to positive response (r = -0.52, P = 0.0032) and the patient age in the entire study population (r = 0.62, P < 0.0001). Results of multiple regression analysis indicated that age, tilt result, and tilt duration were independently associated with the early HR increase. As a result, an early HR increase > or = 18 beats/min, the best apparent cut-off point obtained in our study, was a sensitive (100%) marker for prediction of a positive response at < or = 15 minutes of tilting, but it showed a low specificity (61%). In conclusion, an early HR increase during 80-degree tilting may be only predictive for a positive result < or = 15 minutes because it depends on the tilt duration to a positive response and patient age.

Analysis of heart rate variability during head-up tilt testing in a patient with idiopathic postural orthostatic tachycardia syndrome (POTS).

A 16-year-old boy was diagnosed with idiopathic postural orthostatic tachycardia syndrome (POTS) during head-up tilt testing. During a passive tilt, the patient's heart rate (HR) increased by 30 beats/min within 5 min. After 25 min of tilting, his HR further increased to 133 beats/min and he began to complain of lightheadedness and weakness without hypotension. Power spectral analysis of HR variability during the tilt test revealed that the ratio of low and high frequency powers increased with the onset of orthostatic intolerance. Propranolol (10mg every morning) dramatically alleviated his clinical symptoms, and he has been asymptomatic with gaining weight after discontinuing his crowded train commuting.

Poor reproducibility of false-positive tilt testing results in healthy volunteers.

Positive responses to head-up tilt testing occur in healthy subjects. However, the reproducibility of "false-positive" tilt testing results has not been clarified. To study the reproducibility of "false-positive" responses, we prospectively performed 2 tilt tests separated by 1 to 10 (mean 3.2) weeks in 20 healthy males aged 23 to 40 years (mean 30 years). The baseline tilt test (80 degrees for 30 minutes) ended positive in 4 (20%) subjects on the initial test and 2 (10%) on the second test with only 1 (5%) who had consecutive positive responses. No additional positive responses were noted during the isoproterenol (0.01 microgram/kg/min)-tilt test for 10 minutes. We demonstrated that a false-positive response occurred in 5 (25%) of 20 young males who underwent 2 tilt tests, however, only 1 (5%) subject had consecutive positive responses. Poor reproducibility may be characteristic of false-positive responses in head-up tilt testing.

Response to head-up tilt testing in patients with situational syncope.

The results of head-up tilt testing were compared between 24 patients with situational syncope and 44 age-matched patients with typical vasovagal syncope. Patients with situational syncope showed poor positive responses, especially in the passive tilt results (8.3% vs. 39%, p = 0.0078).

Paroxysmal atrioventricular block induced during head-up tilt testing in an apparently healthy man.

INTRODUCTION: Prolonged asystole during head-up tilt testing has been reported, but the occurrence of paroxysmal AV block appears to be rare. METHODS AND RESULTS: A 25-year-old man with no history of syncope underwent head-up tilt testing. After 11 minutes of 80 degrees tilting, he developed syncope with paroxysmal AV block and asystole lasting 10.5 seconds. However, this response was not reproduced during a subsequent tilt test 4 weeks later. Treadmill exercise testing and Holter monitoring showed no abnormalities. Power spectral analysis of heart rate variability revealed a marked increase in sympathetic activity several minutes before the induction of paroxysmal AV block. CONCLUSION: We report a case of paroxysmal AV block that occurred during head-up tilt testing but did not recur on a subsequent test in an apparently healthy young man.