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Biomedical subjects

F C Lin

Publications and source records attributed to F C Lin.

123 records · Page 7Linked to original sources
PubMed1984

Usefulness of intravenous diltiazem in predicting subsequent electrophysiologic and clinical responses to oral diltiazem.

Diltiazem, 0.25 mg/kg, was given intravenously during induced tachycardias in 6 patients with atrioventricular (AV) nodal reentrant tachycardia (group I) and in 24 patients with AV reentrant tachycardia incorporating a retrogradely conducting accessory pathway (group II). In all 6 group I and in 15 of 24 group II patients, tachycardias terminated within 1 minute after diltiazem administration, with a weak link in the anterograde direction. In 3 other patients in group II, tachycardias were terminated by a premature ventricular complex within 1 minute. In the remaining 6 patients in group II, in whom tachycardias failed to terminate, rates of tachycardias decreased as a result of suppression of anterograde AV nodal conduction by diltiazem. Electrophysiologic studies were performed subsequently 2 hours after the third dose of 90 mg of diltiazem, which was given orally at 8-hour intervals. In 18 responders to intravenous diltiazem who were subjected to oral diltiazem testing, sustained supraventricular tachycardia (SVT) could be induced in only 2. Of the 6 nonresponders, sustained tachycardias could not be induced in 3. Twelve patients, including 11 responders and 1 nonresponder to intravenous diltiazem who responded to oral diltiazem testing, were discharged with oral diltiazem therapy, 90 mg every 8 hours, with follow-up periods of 2 to 13 months (mean 7 +/- 4 [+/- standard deviation]). The frequency of recurrent SVT decreased significantly; 8 patients were free of tachycardias and 4 had occasional recurrences of SVT that required no hospital visit. In conclusion, intravenous diltiazem is effective in terminating SVT. Termination of SVT by intravenous diltiazem predicts subsequent electrophysiologic and clinical responses to oral diltiazem.

Administration, Oral↗
PubMed1984

Determinants of tachycardia induction using ventricular stimulation in dual pathway atrioventricular nodal reentrant tachycardia.

Factors determining tachycardia induction using ventricular stimulation in atrioventricular (AV) nodal reentrant tachycardia utilizing the slow pathway for anterograde and the fast pathway for retrograde conduction were analyzed in 53 patients. Sixteen patients had tachycardia induced by ventricular stimulation. In 15, tachycardia was inducible with incremental ventricular pacing. In 4 of these 15 patients, the tachycardia was also induced with V1V2 testing, while in 11 patients, the tachycardia was not induced with V1V2 testing. In 9 of the latter 11 patients, tachycardia could be induced with V1V2V3 testing, suggesting that the retrograde effective refractory period (ERP) of the right bundle (RB) or the relative refractory period of the His-Purkinje system (HPS) was the limiting factor for tachycardia induction during V1V2 testing. In the remaining one patient, tachycardia was induced with V1V2V3 testing, which provoked a premature ventricular beat, leading to tachycardia induction. Tachycardia was not induced by ventricular stimulation in 37 patients. Factors deterring tachycardia induction in these patients may be related to the retrograde ERP or functional refractory period (FRP) of the HPS, the retrograde ERP of the fast pathway, and an insufficient conduction delay of the circuit (retrograde fast and anterograde slow pathway) to allow anterograde conduction of the slow pathway. In conclusion, AV nodal reentrant tachycardia can be induced by ventricular stimulation in approximately 30% of patients with incremental ventricular pacing and/or ventricular extrastimulus testing. Induction of tachycardia with ventricular stimulation, nevertheless, is frequently limited by the retrograde FRP or ERP of the HPS, the retrograde ERP of the fast pathway, and possibly by an insufficient conduction delay of the circuit.

Adolescent↗
PubMed1983

Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: a unique clinical entity with specific properties.

Electrophysiologic evaluation before and after the serial administration of verapamil, lidocaine, propranolol, and procainamide was undertaken in 4 young, asymptomatic patients with recurrent, sustained ventricular tachycardia (VT). No patient had obvious organic heart disease. The electrocardiogram during sinus rhythm showed S-T depression and T-wave inversion over the inferior and lateral precordial leads in 3 patients. QRS morphologic characteristics during episodes of VT showed a pattern of right bundle branch block and left axis deviation. In all 4 patients, VT could be both induced and terminated with electrical stimulation. Verapamil terminated VT and prevented the induction of sustained VT in 3 patients, and markedly slowed the rate of VT in 1 patient. Procainamide effectively prevented the induction of sustained VT in 2 patients, and although ineffective in preventing induction in 2 patients, it slowed the rate of tachycardia in both. Lidocaine and propranolol did not prevent the induction of VT in any patient. These findings suggest that slow-response tissues may be involved in the genesis of VT in these patients, and that VT in these patients may represent a unique clinical entity with distinct electrocardiographic, electrophysiologic, and electropharmacologic properties.

Adult↗
PubMed1983

Effects of oral diltiazem in paroxysmal supraventricular tachycardia.

Electrophysiologic studies were performed before and 2 hours after the oral administration of 270 mg of diltiazem in 3 divided doses at 8-hour intervals in 36 patients with paroxysmal supraventricular tachycardia (SVT). Before diltiazem, all 36 patients had induction of sustained SVT: 24 with atrioventricular (AV) reentrance incorporating an accessory pathway (Group 1) and 12 with AV nodal reentrance (Group 2). After diltiazem, 20 patients in Group 1 lost the ability to induce or sustain SVT because of increased anterograde normal pathway refractoriness in 19 patients and increased retrograde accessory pathway refractoriness in 1. Eight patients in Group 2 could no longer induce or sustain SVT because of increased anterograde slow pathway refractoriness in 2 patients and increased retrograde fast pathway refractoriness in 6. Diltiazem concentration in the blood, measured in 29 patients, was 156 +/- 75 ng/ml (mean +/- standard deviation). Fifteen patients, 2 with and 13 without induction of sustained SVT after diltiazem, were discharged on the same dosage of diltiazem and followed up 5 +/- 3 months. The former 2 patients had attacks of sustained SVT, whereas the latter 13 have been free of sustained SVT. In conclusion, oral diltiazem prevents induction and sustenance of paroxysmal SVT in most patients and may be used as an alternative agent for the prophylaxis of SVT.

Administration, Oral↗
PubMed1983

Effects of oral verapamil in patients with atrioventricular reentrant tachycardia incorporating an accessory pathway.

In 14 patients with atrioventricular reentrant tachycardia incorporating an accessory pathway, electrophysiologic studies were performed before and serially at 0.5--1-hour intervals for 6 hours after the fourth dose of 80 mg of oral verapamil given every 6 hours. Verapamil increased both the longest atrial paced cycle length producing type 1 atrioventricular block and the effective refractory period of the atrioventricular conduction system at all measurements. Before verapamil, sustained tachycardia could be induced in all 14 patients. After verapamil, six patients had induction of echo beats alone at all measurements, and in eight patients nonsustained or sustained tachycardia could be induced, particularly after the fourth hour. Follow-up study with oral verapamil at the same dosage in 13 patients for 7 +/- 5 months (+/- SD) revealed that the six patients with induction of echo beats alone have been free of symptomatic arrhythmia, while six of the remaining eight patients had occasional attacks of sustained tachycardia. Thus, oral verapamil increases atrioventricular nodal refractoriness, with an effect lasting up to 6 hours. Electrophysiologic study performed 5-6 hours after verapamil can be used to predict clinical responses in patients with atrioventricular reentrant tachycardia.

Administration, Oral↗
PubMed1983

Effects of acebutolol on paroxysmal atrioventricular reentrant tachycardia in patients with manifest or concealed accessory pathways.

Electrophysiologic studies before and after administration of 50 mg of intravenous (IV) acebutolol were performed in 20 patients. Four of the 20 had persistent preexcitation, two had intermittent preexcitation, and 14 had a concealed retrogradely conducting accessory pathway (AP). Acebutolol depressed anterograde AP conduction with loss of preexcitation in one patient and increased the effective refractory period of AP in the remaining three; in most, it depressed anterograde normal pathway conduction. The longest atrial paced cycle length producing atrioventricular (AV) nodal block increased from 290 +/- 7 to 39 +/- 6 msec (mean +/- SEM) after acebutolol (p less than 0.01). Acebutolol had no significant effect on retrograde AP conduction. Sustained AV reentrant tachycardia was inducible in all 20 patients before acebutolol and in 19 after acebutolol. The cycle length of tachycardia increased from 323 +/- 8 to 352 +/- 8 msec after acebutolol (p less than 0.01), reflecting an increment of A-H interval from 148 +/- 8 to 174 +/- 9 msec (p less than 0.01). Electrophysiologic studies were reported after 800 mg of oral acebutolol given in four divided doses at six-hour intervals in eight patients. The results were comparable to those of IV acebutolol. Thus, acebutolol depresses AV nodal conduction and slows the rate of AV reentrant tachycardia, but is generally ineffective in inhibiting the induction of sustained tachycardia. It occasionally depresses anterograde AP conduction.

Acebutolol↗
PubMedDate not supplied

Doppler atrial shunt flow patterns in patients with secundum atrial septal defect: determinants, limitations, and pitfalls.

Fifteen patients with uncomplicated secundum atrial septal defect underwent studies with real-time color-coded two dimensional flow imaging, pulsed Doppler echocardiographic examination, and simultaneous pressure recordings from the left and right atrium to determine the flow-pressure dynamics of the atrial shunt flow. In all 15 patients both the color flow mapping and pulsed Doppler studies revealed that the shunt flow was mainly from left to right, occurring both during ventricular systole and diastole. It started in early systole, reached a peak in late systole to early diastole, and lasted throughout diastole with an accentuation in late diastole during atrial contraction. The amplitude of the flow velocity, the direction, and the magnitude of the shunt flow, however, changed from phase to phase during the cardiac cycle. It correlated well with the phasic variation of the interatrial pressure difference, which usually revealed a peak pressure gradient that occurred in early systole between the x descent and v wave and during the period of v wave and a wave of the left atrial pressure tracing. Right to left shunt was not detected in any of the 15 patients by color flow mapping studies. A minor reversal of the shunt flow, however, was frequently detected at the beginning of ventricular systole and sometimes also in the middle of diastole by pulsed Doppler echocardiography. The reversal of shunt flow correlated with the minor reversal of pressure gradient that occurred during the z point, x descent, and y descent of the left atrial pressure tracing. In conclusion, left to right shunt flow occurs both during ventricular systole and diastole in uncomplicated secundum atrial septal defect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Postoperative echocardiographic study of patients with symptomatic chronic aortic regurgitation.

Aortic valve replacement was performed in 31 patients with symptomatic chronic aortic regurgitation. The patients ranged in age from 13 to 66 (mean = 39) years and included 29 men and 2 women. They were followed up for a mean of 47 months. Perioperatively, 2 patients (6.5%) died, and 2 (6.5%) received a permanent pacemaker for complete heart block. Thirty patients received an M-mode echocardiographic examination both before, and 6 to 11 days after, the operation. In this early postoperative period, the end-diastolic dimension (EDD) and left ventricular end-diastolic radius/posterior wall thickness ratio (R/Th) decreased in all patients. This decrease in EDD could be predicted by preoperative ejection fraction (EF), but not by end-systolic dimension (ESD) or R/Th ratio. The ESD regressed only in patients with preoperative EF greater than 50%, or ESD less than 55mm, or R/Th less than 3.8. During the long-term follow-up, one each had mild tissue valve degeneration, stroke, infective endocarditis, and severe myocardial failure, but none died. Eighteen patients had repeated M-mode echocardiographic studies. There was no further regression of EDD and R/Th, while ESD showed significant decrease. The EF and fractional shortening (FS) did not change. Clinically, the patients who survived the operation improved or remained unchanged postoperatively in a functional status. However, those who had preoperative EF greater than 50% or ESD less than 55mm had a better postoperative functional class (1.2 +/- 0.4 vs 1.9 +/- 1.0, p less than 0.05, 1.2 +/- 0.4 vs 2.0 +/- 1.1, p less than 0.05, respectively). Thus, patients with symptomatic chronic aortic regurgitation can often benefit from valve replacement.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗