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Compared to age-matched normotensive adults, those with essential hypertension have been shown to have distinct arterial hemodynamic abnormalities consisting of increased peripheral resistance, pulse wave velocity, and wave reflection magnitude as well as decreased wave reflection time and aortic compliance. These abnormalities are further exacerbated by beta-adrenergic blockade. To see if there are similar hemodynamic abnormalities that antedate the onset of fixed hypertension, we compared age-matched normotensives with prehypertensives selected from patients undergoing diagnostic cardiac catheterization. Ascending aortic pressure and flow were measured with a micromanometer and flow velocity sensor in the baseline state and after beta-adrenergic blockade. In the baseline state the prehypertensive compared to the normotensive group had elevated blood pressure, resistance, left ventricular end-diastolic pressure (LVEDP), and wave reflections. Beta-adrenergic blockade increased resistance, LVEDP, and wave reflections in both groups. Some of these findings are the same as those we previously reported in young persons with established, essential hypertension. The differences in LVEDP and wave reflections, both in the baseline state and after beta-blockade, were still present in subgroups with no differences in blood pressure. Hence, the elevated wave reflections in prehypertensives do not appear to be directly related to the level of blood pressure. These results support the notion that the elevated blood pressure in hypertension may represent a later manifestation of an already abnormal vascular system rather than the vascular abnormalities resulting from hypertension. Consequently, even before blood pressure becomes elevated, early diagnosis and treatment of the vascular abnormalities in prehypertensives may be warranted. [ABSTRACT FROM AUTHOR]

The coronary arteries are the major blood vessels supplying the heart, and under abnormal conditions, they may become narrowed or obstructed resulting in myocardial ischemia, the insufficient supply of blood to the heart. Coronary artery disease (CAD) may be associated with specific abnormalities in the electrical activity of the heart, as recorded by electrocardiography (ECG). Under normal conditions, the septal Q wave in the electrical record increases in amplitude during exercise, but this is not observed in patients with coronary artery disease. Studies have suggested that the abnormality in the septal Q wave may be associated with ischemia of the septum, the wall separating the right and left ventricles. Septal ischemia may result from narrowing of the left anterior descending coronary artery (LAD). This study examined the septal Q wave during exercise in 38 CAD patients, half of whom had LAD narrowing close to the septal blood vessels and a decreased blood supply to the septum. The results demonstrate that the occurrence of an abnormal Q wave was significantly correlated with narrowing or stenosis of the LAD close to the septal blood supply. Angioplasty, a procedure to repair the affected coronary artery, temporarily eliminated the abnormal Q wave in only eight of 19 patients with an abnormal Q wave. The results show that LAD narrowing decreases the blood supply to the septum causing septal ischemia during exercise and the occurrence of abnormal Q waves. (Consumer Summary produced by Reliance Medical Information, Inc.)

TAI, C.T., et al.: Conduction Properties of the Crista Terminalis in Patients with Atrial Flutter Due to Amiodarone Therapy for Atrial Fibrillation. Some patients with atrial fibrillation (AF) treated by antiarrhythmic drugs (AAD) can develop typical atrial flutter, but the mechanism is not clear. This study included 21 patients with AF. Group I (n = 7) had typical atrial flutter due to amiodarone therapy. Group II (n = 7) did not develop atrial flutter after amiodarone treatment. Group III (n = 7) did not receive AAD treatment. A 7 Fr, 20-pole electrode catheter was placed along the CT identified by fluoroscopy and intracardiac echocardiography. After restoration of the sinus rhythm, decremental pacing near the CT was performed until 2 to 1 atrial capture. Complete transverse conduction block was defined as the appearance of double potentials with opposite activation sequence along the CT. Focal transverse conduction delay was defined as the appearance of double potentials at ≥ 2 recording sites. Focal transverse conduction delay was observed during pacing at the cycle length of 693 ± 110 ms in group I, 360 ± 97 ms in group II and 343 ± 109 ms in group III (P = 0.001). Complete transverse conduction block was observed during pacing at the cycle length of 391 ± 118 ms in group I and 231 ± 23 ms in group II (P = 0.001), but not in group III. In conclusion, focal transverse conduction delay in the CT was common in patients with AF. A predisposition to the line of the conduction block in the CT might contribute to the conversion of AF to typical atrial flutter due to amiodarone therapy. (PACE 2003; 26:2241–2246) [ABSTRACT FROM AUTHOR]

Spontaneous Transition of 2:1 AV Block to 1:1 AV Conduction. Introduction: The incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction during AV nodal reentrant tachycardia has not been well reported. Among previous studies, controversy also existed about the site of the 2:1 AV block during AV nodal reentrant tachycardia. Methods and Results: In patients with 2:1 AV block during AV nodal reentrant tachycardia, the incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction and change of electrophysiologic properties during spontaneous transition were analyzed. Among the 20 patients with 2:1 AV block during AV nodal reentrant tachycardia, a His-bundle potential was absent in blocked beats during 2:1 AV block in 8 patients, and the maximal amplitude of the His-bundle potential in the blocked beats was the same as that in the conducted beats in 4 patients and was significantly smaller than that in the conducted beats in 8 patients (0.49 ± 0.25 mV vs 0.16 ± 0.07 mV, P = 0.007). Spontaneous transition of 2:1 AV block to 1:1 AV conduction occurred in 15 (75%) of 20 patients with 2:1 AV block during AV nodal reentrant tachycardia. Spontaneous transition of 2:1 AV block to 1:1 AV conduction was associated with transient right and/or left bundle branch block. The 1:1 AV conduction with transient bundle branch block was associated with significant His-ventricular (HV) interval prolongation (66 ± 19 ms) compared with 2:1 AV block (44 ± 6 ms, P < 0.01) and 1:1 AV conduction without bundle branch block (43 ± 6 ms, P < 0.01). Conclusion: The 2:1 AV block during AV nodal reentrant tachycardia is functional; the level of block is demonstrated to be within or below the His bundle in a majority of patients with 2:1 AV block during AV nodal reentrant tachycardia, and a minority are possibly high in the junction between the AV node and His bundle. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1337-1341, December 2003) [ABSTRACT FROM AUTHOR]

Very Late Recurrence of AF. Introduction: High recurrence rate is still a major problem associated with ablation of paroxysmal atrial fibrillation (AF). Most of the recurrences occur within 6 months after ablation. The characteristics of very late recurrent AF (>12 months after ablation) have not been reported. Methods and Results: Two hundred seven patients with drug-refractory AF underwent successful focal ablation or isolation of AF foci. After the first ablation procedure, Holter monitoring and event recorders were used to evaluate symptomatic recurrent AF. A second ablation procedure was recommended if the antiarrhythmic drugs could not control recurrent AF. During long-term follow-up (mean 30 ± 11 months, up to 51 months), 70 patients had recurrent AF, including 13 patients (6%) with very late (>12 months) recurrent AF (group 1) and 57 patients (28%) with late (within 12 months after ablation) recurrent AF(group 2). Group 1 patients had a significantly lower incidence of multiple (≥2) AF foci (23% vs 63%, P = 0.02) than group 2 patients. In addition, the incidence of antiarrhythmic drugs use (38% vs 84%, P = 0.001) to maintain sinus rhythm after the first episode of recurrent AF was significantly lower in group 1 than group 2 patients, and the incidence of a second intervention procedure (8% vs 35%, P = 0.051) tended to be lower in group 1 than group 2 patients. Conclusion: The incidence of very late recurrent AF after ablation of paroxysmal AF is very low, and the clinical outcome of patients with very late recurrent AF is benign.(J Cardiovasc Electrophysiol, Vol. 14, pp. 598-601, June 2003). [ABSTRACT FROM AUTHOR]

: BackgroundOur understanding of genes that predispose to essential hypertension is poor.: MethodsA genome-wide scan for linkage at ∼10 cM resolution was done on 1425 sibpairs of Chinese and Japanese origins that were concordant for hypertension (N = 661), low–normal blood pressure (BP) (N = 184), or discordant for BP (N = 580).: ResultsThere was no significant evidence of linkage to a single locus in the genome. There was suggestive evidence of linkage to chromosome 10p, with a LOD score of 2.5.: ConclusionsWe can exclude the possibility that a single gene accounts for at least 15% of the variance in hypertension in this population. [Copyright &y& Elsevier]

CHEN, J.‐W., et al.: Impairment of Coronary Microvascular Function in Patients with Neurally Mediated Syncope.Recent evidence suggests that myocardial ischemia may occur in patients with neurally mediated syncope and normal coronary angiograms. This study was conducted to evaluate if coronary microvascular function is impaired in such patients. Coronary hemodynamic studies and head‐up tilt table tests (HUTs) were performed on 30 consecutive patients with normal coronary angiograms and recurrent syncope. Another ten subjects with atypical chest pain and no evidence of myocardial ischemia or syncope served as a control. Great cardiac vein flow (GCVF) and coronary sinus flow (CSF) were measured by the thermodilution method at baseline and after dipyridamole infusion (0.56 mg/kg IV for 4 minutes). Coronary flow reserve (CFR), derived from CSF and GCVF, was significantly lower in the 15 patients with positive HUT than in the other 15 patients with negative HUT (1.75 ± 0.48vs2.64 ± 0.8, P < 0.01and2.29 ± 0.45vs3.07 ± 0.63, P < 0.01, respectively). Ischemic‐like ECG was noted during treadmill exercise test in 40% of the former and in 7% of the latter group(P = 0.01). There was no significant difference in CFR between patients with negative HUT and control subjects. Coronary microvascular function was impaired in syncopal patients with positive HUT and relatively preserved in those with negative HUT, suggesting the possible linkage between coronary microvascular dysfunction and the development of neurally mediated syncope. (PACE 2003; 26[Pt. I]:605–612) [ABSTRACT FROM AUTHOR]

Objective: Pulmonary veins are important foci of ectopic beats to initiate paroxysmal atrial fibrillation. The purpose of this study were to investigate the electrophysiological characteristics of excitable cells in canine pulmonary veins obtained from healthy and chronic rapid atrial pacing dogs and their responses to cardioactive agents. Methods: Transmembrane action potentials (APs) were recorded from multiple sites of pulmonary veins isolated from 17 healthy dogs and 14 dogs with chronic (6–8 weeks) rapid atrial pacing (780 bpm). Results: In normal superfusate, several types of electrical activities were identified, including silent electrical activity, fast response APs driven by electrical stimulation, and spontaneous fast or slow response APs (with or without early afterdepolarizations). The incidences of AP with an early afterdepolarization (93% versus 41%) was greater in chronic pacing dogs. The spontaneous activities were depressed by beta-adrenoceptor blocker, calcium channel blocker, adenosine and acetylcholine. High frequency (<8 Hz) irregular rhythms occurred spontaneously or were induced by cardioactive agents or electrical stimuli. The incidence of spontaneously occurring tachyarrhythmias was much higher in preparations from chronic pacing dogs (93%) than from control (12%). The tachyarrhythmias were suppressed by sodium channel blocker, potassium channel blocker or magnesium. Conclusions: Pulmonary veins have arrhythmogenic ability through spontaneous activities or high-frequency irregular rhythms. The higher incidence of spontaneously occurring high-frequency irregular rhythms in chronic rapid atrial pacing dogs may account for the increased risk of atrial fibrillation in these dogs. [ABSTRACT FROM PUBLISHER]

Background: In animal studies, atrial fibrillation has been shown to shorten the atrial refractory period and impair its rate adaptation. However, little is known about the effects of chronic atrial fibrillation on atrial electrophysiology and its recovery course in humans. Methods and results: Nineteen patients, mean age 64±14 years, with chronic atrial fibrillation of more than six months duration were included in this study. All of them were successfully converted to sinus rhythm with an external defibrillator. Atrial effective refractory periods at right atrial appendage and distal coronary sinus were determined with five pacing cycle lengths (300, 400, 500, 600 and 700 ms) at 30 min after cardioversion and once a day for four days. The atrial conduction properties, including P wave duration of surface ECG, and right and left atrial conduction times, were also measured at the same time interval. Twenty age-matched patients without a history of atrial tachyarrhythmia were evaluated as controls. In comparison with controls, chronic atrial fibrillation significantly shortened the atrial effective refractory period, impaired its rate adaptation response, especially at distal coronary sinus, and depressed the conduction properties of atria. The atrial conduction properties did not change during the four-day follow-up period; however, the atrial effective refractory period was gradually prolonged and its rate adaptation response improved after restoration of sinus rhythm. Conclusions: In humans, chronic atrial fibrillation significantly shortened the atrial effective refractory period, and impaired its rate adaptation response. Restoration and maintenance of sinus rhythm could reverse these electrophysiological changes. [ABSTRACT FROM PUBLISHER]