Douglas C. Westveer

Paroxysmal atrial fibrillation in the wolff-parkinson-white syndrome

Eighty-eight patients with preexcitation were studied to determine how 30 patients with documented spontaneous paroxysmal atrial fibrillation differed from 58 patients without this arrhythmia. Inducible reentrant tachycardia was present in 23 (77 percent) of the 30 patients with, versus 28 (48 percent) of the 58 patients without, atrial fibrillation (p less than 0.025). Heart disease was present in 13 (43 percent) of the 30 patients with, versus 15 (26 percent) of the 58 patients without, atrial fibrillation (not significant). Inducible reentrant tachycardia or heart disease, or both, were significant). Inducible reentrant tachycardia or heart disease, or both, were present in 29 (97 percent) of the 30 patients with, versus 34 (59 percent) of the 58 patients without, atrial fibrillation (p less than 0.0005). Of 51 patients with inducible reentrant tachycardia, 23 patients with atrial fibrillation did not differ from 28 patients without this arrhythmia with respect to clinical features and atrial, sinus nodal, or anomalous pathway properties, or cycle length of induced reentrant tachycardia. Spontaneous degeneration of induced reentrant tachycardia to atrial fibrillation was observed in 6 (26 percent) of 23 patients with, versus none of 28 patients without, atrial fibrillation (p less than 0.025). In summary, patients with preexcitation and documented spontaneous paroxysmal atrial fibrillation almost always have inducible reentrant tachycardia or heart disease, or both. It is likely that in many patients with inducible reentrant tachycardia, spontaneously occurring reentrant tachycardia relates to induction of atrial fibrillation. However, it is unclear why some patients with inducible reentrant tachycardia have atrial fibrillation and others do not. In many patients with organic heart disease, atrial fibrillation could relate to hemodynamic changes.

Sequelae of left ventricular electrical endocardial ablation

The endomyocardial residual effects of left ventricular endocardial electrical ablation utilizing unipolar and bipolar electrode catheters were studied in 15 dogs. Histopathologic techniques specific for contraction band necrosis revealed that the mean maximal depth and breadth of necrosis was 0.63 +/- 0.44 and 1.23 +/- 0.82 cm, respectively. The dimensions of necrosis were significantly increased when utilizing larger energy discharges, especially through unipolar electrodes. Four dogs died during the procedure, three from ventricular fibrillation and one from asystole, and two died suddenly within the succeeding 24 hours. Endocardial thrombi were noted at necropsy in two dogs. In conclusion, transcatheter endocardial electrical ablation may destroy a sufficient mass of myocardium to interrupt arrhythmogenic conduction tissue, especially when larger currents are delivered through unipolar electrodes. However, serious ventricular arrhythmias and endocardial thrombi should be anticipated.

Aneurysm of the atrial septum as diagnosed by echocardiography: Analysis of 11 patients

Atrial septal aneurysm (ASA) is considered uncommon and, when discovered, has usually been found in association with other cardiac lesions.1-4 This association has led some observers to conclude that their occurrence is the result of an increased pressure gradient between the atria producing a bulging septal shift toward the low pressure side.1*2 In contrast, Silver and Dorsey5 detected clinically silent aneurysm of the septum primum in 16 of 1,578 serially autopsied adults. Only 1 of their 5 hemodynamically studied patients had elevated left ventricular end-diastolic pressure. Atrial septal aneurysm has been found by 2dimensional echocardiography (2-D echo) in association with various congenital and acquired valvular diseases.334 A patient who had a myocardial infarction and ASA with phasic inspiratory right-to-left motion of the aneurysm was reported.6 Isolated case reports of ASA associated with a midsystolic click,7 and with no associated lesions,” have also been recently reported. The subject of our report is 11 cases of ASA shown by 2-D echo to exist in the absence of other identifiable structural cardiac abnormalities.

Amiodarone-lnduced Ventricular Tachycardia

Excerpt Virtually all antiarrhythmic agents may facilitate ventricular tachycardia. However, amiodarone has been free of this adverse effect, except in two cases where it was used in combination wi...

Worsening of ventricular tachycardia by amiodarone

The details of worsening of ventricular tachycardia in 8 (4.1%) of 194 patients receiving treatment with amiodarone are reported. Two forms of amiodarone‐induced tachycardia were recognized: first, the development of new tachycardias (three patients) and second, a change in the pattern of recurrence of clinical tachycardia (five patients). In retrospect, the time from the initiation of amiodarone to the initial documentation of worsening ranged from 1 to 23 days (mean ± SD, 9.4 ± 8.2 days) and the time from the initiation of therapy to the recognition of worsening ranged from 6 to 26 days (14.6 ± 10.1 days). Seven patients survived the worsening of tachycardia and one died. The total dose of amiodarone received and the duration of administration did not correlate with time to manifestation or time to resolution of worsening. This report emphasizes that worsening of ventricular tachycardia as a result of amiodarone is often difficult to differentiate from inadequate drug loading or early recurrence of 2 patients clinical tachycardia. Further, because of the pharmacokinetics of the drug, the manifestations of worsening may be prolonged. In the cases reported, it ranged from 2 to 26 days (7.9 ± 8.3 days), which is longer than previously reported. Because of the potential for amiodarone to cause life‐threatening worsening of ventricular tachycardia and in accordance with current results, a period of in‐hospital monitoring of at least 10 days at the start of therapy with amiodarone is recommended.