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Biomedical subjects

F C Lin

Publications and source records attributed to F C Lin.

At least 91 records · Page 5Linked to original sources
PubMed1991

Repetitive sinoatrial exit block as the major mechanism of drug-provoked long sinus or atrial pause.

Prolonged sinus or atrial pause occurred in six patients with paroxysmal supraventricular tachycardia after drug administration. All six patients had normal sinus node function during control electrophysiologic study; the sinus cycle length ranged from 510 to 900 ms (mean 743 +/- 141) and the longest sinus node recovery time ranged from 800 to 1,230 ms (mean 1,018 +/- 168). A long sinus or atrial pause occurring at the termination of tachycardia or cessation of atrial pacing, ranging from 3,100 to 8,200 ms (mean 6,270 +/- 1,674), was provoked by the administration of various drugs. These included an intravenous bolus injection of adenosine triphosphate (5 mg; one patient), intravenous bolus injection of verapamil (5 mg; one patient), a combination of a single oral dose of diltiazem (120 mg) and propranolol (20 to 40 mg; three patients), oral diltiazem (240 mg/day; one patient) and a combination of oral diltiazem (240 mg/day) and propranolol (160 mg/day; one patient). In five patients, low frequency deflections suggestive of sinus node activity with a cycle length between 620 and 3,500 ms were recorded during pauses. These findings suggest that repetitive sinoatrial exit block was responsible for the pause. Sinus slowing with a long arrest suggesting suppression of sinus automaticity was also noted in three of these five patients; the longest sinus arrest in these three patients was 4,160, 4,800 and greater than 4,910 ms, respectively. The remaining patient with a pause of 6,840 ms had no recordable sinus activity, either reflecting suppression of sinus automaticity or technical failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1991

Familial patent ductus arteriosus. Report of a family.

Three female patients of two generations in one family each had patent ductus arteriosus (PDA) that was proved by echocardiography and cardiac catheterization. Two of them received surgical ligation of the PDA because of large left to right shunt (Qp/Qs of 3.8 and 2.7, respectively), while the third patient with a Qp/Qs of 1.2 was not operated. Although the exact cause of PDA in this family is unclear, an autosomal recessive inheritance is highly possible.

Child↗
PubMed1990

Effects of isoproterenol on accessory pathway conduction in intermittent or concealed Wolff-Parkinson-White syndrome.

The effects of isoproterenol on accessory pathway conduction were evaluated in 24 patients with intermittent and 60 patients with concealed pre-excitation, using atrial and ventricular incremental and extrastimulus testing techniques. The atrial paced cycle length that induced block in the accessory pathway could be compared in 11 of the 24 patients with intermittent preexcitation before and after isoproterenol; it decreased from 622 +/- 212 ms to 408 +/- 128 ms (mean +/- standard deviation) after isoproterenol (p less than 0.01). The anterograde effective refractory period of the accessory pathway could be compared in 5 patients before and after isoproterenol; it decreased from 460 +/- 131 to 310 +/- 48 ms after isoproterenol (p less than 0.01). None of the 60 patients with concealed preexcitation showed ventricular preexcitation with isoproterenol infusion. Eighty-one of the 84 patients had clinically documented supraventricular tachycardia, suggesting the accessory pathway was capable of retrograde conduction. Retrograde study was performed in all 84 patients; 83 had retrograde conduction and the other had no retrograde conduction before and after isoproterenol. The ventricular paced cycle length that induced block in the accessory pathway could be compared in 38 patients before and after isoproterenol; it decreased from 342 +/- 71 to 296 +/- 39 ms after isoproterenol (p less than 0.001). The retrograde effective refractory period of the accessory pathway could be compared in 56 patients; it decreased from 293 +/- 76 to 238 +/- 36 ms after isoproterenol (p less than 0.001). In conclusion, isoproterenol facilitates anterograde and retrograde accessory pathway conduction, but the facilitation of anterograde conduction occurs only in those capable of spontaneous conduction.

Adolescent↗
PubMed1990

Identification of the uridine 5'-diphosphoglucose (UDP-Glc) binding subunit of cellulose synthase in Acetobacter xylinum using the photoaffinity probe 5-azido-UDP-Glc.

Photoaffinity labeling of purified cellulose synthase with [beta-32P]5-azidouridine 5'-diphosphoglucose (UDP-Glc) has been used to identify the UDP-Glc binding subunit of the cellulose synthase from Acetobacter xylinum strain ATCC 53582. The results showed exclusive labeling of an 83-kDa polypeptide. Photoinsertion of [beta-32P]5-azido-UDP-Glc is stimulated by the cellulose synthase activator, bis-(3'----5') cyclic diguanylic acid. Addition of increasing amounts of UDP-Glc prevents photolabeling of the 83-kDa polypeptide. The reversible and photocatalyzed binding of this photoprobe also showed saturation kinetics. These studies demonstrate that the 83-kDa polypeptide is the catalytic subunit of the cellulose synthase in A. xylinum strain ATCC 53582.

Affinity Labels↗
PubMed1990

Cloning and sequencing of the cellulose synthase catalytic subunit gene of Acetobacter xylinum.

The gene for the catalytic subunit of cellulose synthase from Acetobacter xylinum has been cloned by using an oligonucleotide probe designed from the N-terminal amino acid sequence of the catalytic subunit (an 83 kDa polypeptide) of the cellulose synthase purified from trypsin-treated membranes of A. xylinum. The gene was located on a 9.5 kb Hind III fragment of A. xylinum DNA that was cloned in the plasmid pUC18. DNA sequencing of approximately 3 kb of the Hind III fragment led to the identification of an open reading frame of 2169 base pairs coding for a polypeptide of 80 kDa. Fifteen amino acids in the N-terminal region (positions 6 to 20) of the amino acid sequence, deduced from the DNA sequence, match with the N-terminal amino acid sequence obtained for the 83 kDa polypeptide, confirming that the DNA sequence cloned codes for the catalytic subunit of cellulose synthase which transfers glucose from UDP-glucose to the growing glucan chain. Trypsin treatment of membranes during purification of the 83 kDa polypeptide cleaved the first 5 amino acids at the N-terminal end of this polypeptide as observed from the deduced amino acid sequence, and also from sequencing of the 83 kDa polypeptide purified from membranes that were not treated with trypsin. Sequence analysis suggests that the cellulose synthase catalytic subunit is an integral membrane protein with 6 transmembrane segments. There is no signal sequence and it is postulated that the protein is anchored in the membrane at the N-terminal end by a single hydrophobic helix. Two potential N-glycosylation sites are predicted from the sequence analysis, and this is in agreement with the earlier observations that the 83 kDa polypeptide is a glycoprotein. The cloned gene is conserved among a number of A. xylinum strains, as determined by Southern hybridization.

Amino Acid Sequence↗
PubMed1990

Participation of a concealed nodoventricular fiber in the genesis of paroxysmal tachycardias.

An unusual form of tachycardia circuit is described. The circuit incorporates a concealed nodoventricular fiber that conducts in a retrograde path, connects the atrioventricular node and the right ventricle, and also includes the distal portion of the atrioventricular node, the His-Purkinje system, and the ventricle. The study patient was first seen with paroxysmal tachycardias of normal QRS duration, complete right bundle branch block, and complete left bundle branch block. Electrophysiologic studies disclosed poor anterograde atrioventricular nodal conduction with a block proximal to His deflection that occurred at an atrial paced cycle length of 600 msec with no ventriculoatrial conduction. The tachycardias were inducible with two ventricular extrastimuli, had a His deflection that preceded each QRS complex and an HV interval identical to that during sinus rhythm, and revealed ventriculoatrial dissociation. Tachycardia with QRS patterns of right bundle branch block had a cycle 30 to 35 msec longer than tachycardias with either normal QRS duration or complete left bundle branch block. Tachycardias could be entrained by appropriate right ventricular pacing at rates slightly faster than the rate of tachycardia. Tachycardias could be terminated abruptly by an intravenous bolus of either adenosine triphosphate or verapamil.

Bundle-Branch Block↗
PubMed1990

Atrioventricular block in the atypical form of junctional reciprocating tachycardia: evidence supporting the atrioventricular node as the site of reentry.

Serial electrophysiologic studies were performed in 19 patients with the atypical form of supraventricular tachycardia having a long RP and short PR interval. In all 19 patients, supraventricular tachycardia was found to have a 1:1 P-QRS relation during initial control electrophysiologic studies, and in all 19 patients, electrophysiologic studies suggested that junctional reentry was the mechanism of supraventricular tachycardia. Seven of the 19 patients developed atrioventricular (AV) block during initiation of supraventricular tachycardia or after induction of supraventricular tachycardia following various drug administrations in subsequent studies. In three patients, second degree block within the His bundle or block distal to the His bundle recording site occurred after administration of quinidine. In one patient it occurred after procainamide, and in another patient it occurred after atropine. In one patient, 2:1 block proximal to the His deflection occurred after verapamil. In the remaining patient, a transient Wenckebach block proximal to the His deflection was noted after adenosine triphosphate. In this latter patient, 2:1 AV block was also noted after propranolol and digoxin. The site of reentry in these seven patients with AV block during supraventricular tachycardia was confined to the AV node area. Their supraventricular tachycardia did not involve a slowly conducting paraseptal accessory pathway because the distal AV node, His bundle and ventricle were not found to be necessary links in the tachycardia circuit.

Adolescent↗
PubMed1990

Two-dimensional and Doppler echocardiographic features of coronary arteriovenous fistula. Report of three cases.

Two-dimensional (2-D) and Doppler echocardiographic features of three cases of coronary arteriovenous fistula (CAVF) were analyzed. The final diagnosis was confirmed by coronary angiography in each case. In cases 1 and 2, the CAVF arose from the right coronary artery and drained into the right atrium and right ventricle, respectively. The origin and draining site of the CAVF could be visualized by 2-D echocardiograms. The Doppler studies revealed a unidirectional flow within the lumen of the CAVF. In case 3, with a small CAVF originating from both the right coronary artery and left circumflex artery draining into the main pulmonary artery, no abnormal vascular structure could be detected by the 2-D echocardiogram; with Doppler study, a diastolic as well as systolic flow signal directed toward the distal pulmonary artery could be detected.

Adult↗
PubMed1990

Hemodynamic and clinical efficacies of catheter balloon percutaneous transvenous mitral commissurotomy: experience of 100 patients with rheumatic mitral stenosis.

From January 1987 to December 1988, 100 patients with symptomatic severe rheumatic mitral stenosis underwent percutaneous transvenous mitral commissurotomy (PTMC). The patients included 32 males and 68 females, aged 19-71 years (mean of 41). Mild mitral regurgitation (grade 1 or 2) was present in 23 patients and a history of thromboembolism in 12. One patient had had mitral restenosis after surgical open mitral commissurotomy 9 years earlier. The mitral valve was successfully dilated in 97 patients. PTMC resulted in immediate improvements in hemodynamic measurements. The left atrial pressure decreased from 24.5 +/- 5.3 to 14.8 +/- 5.2 mmHg (p less than 0.001), the mean mitral transvalvular gradient from 13.8 +/- 4.8 to 5.0 +/- 2.8 mmHg (p less than 0.001), and the mean pulmonary artery pressure from 38.8 +/- 12.0 to 30.6 +/- 10.3 mmHg (p less than 0.001). The mitral valve area increased from 1.1 +/- 0.3 to 2.2 +/- 0.8 cm2 (p less than 0.001). The cardiac output increased from 4.5 +/- 1.2 to 4.84 +/- 1.2 L/min (p less than 0.05). The right atrial pressure did not change significantly after PTMC (6.5 +/- 3.8 vs 6.4 +/- 4.0 mmHg). The mitral valve area measured by 2-D echocardiograms increased from 1.04 +/- 0.48 to 1.88 +/- 0.66 cm2 after PTMC (p less than 0.001). All 97 patients were followed for 6-24 months (median of 13) after the PTMC. After an initial recovery period of 1-2 weeks, all patients reported improvements in symptoms and in New York Heart Association (NYHA) functional class by at least one class. A comparison between treadmill exercise test durations before, and 3 months after PTMC, showed an increase from 9.1 +/- 4.3 to 15.4 +/- 3.8 minutes (n = 60; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

The mechanisms of exercise provocation of supraventricular tachycardia.

Treadmill exercise tests, electrophysiologic studies, and isoproterenol infusions were performed in 14 patients with exercise provocable supraventricular tachycardia to delineate the mechanisms of exercise provocation of paroxysmal supraventricular tachycardia. Treadmill exercise tests reproducibly provoked supraventricular tachycardia in all patients. Supraventricular tachycardia similar to that provoked by exercise occurred spontaneously during isoproterenol infusions in 9 of 11 patients tested. The specific supraventricular tachycardia diagnoses of all patients were atrial reentrant tachycardia (two patients), automatic atrial tachycardia (three), atrial flutter-fibrillation (one), atypical junctional tachycardia (two), and orthodromic atrioventricular (AV) reentrant tachycardia (six) as defined by electrophysiologic studies. Various mechanisms of exercise or isoproterenol induction of supraventricular tachycardia were identified. A critical heart rate and/or appropriate sympathetic state was found to provoke all instances of reentrant or automatic atrial tachycardia and atypical junctional tachycardia. A properly timed atrial premature beat provoked five of six cases of AV reentrant tachycardia and the only case of atrial flutter-fibrillation. The remaining case of AV reentrant tachycardia was induced by a ventricular premature beat. In conclusion, the mechanisms of exercise provocation of reentrant or automatic supraventricular tachycardia are multiple and include a critical sinus rate, increased sympathetic tone, and properly timed atrial or ventricular premature beats.

Adrenergic beta-Agonists↗
PubMed1989

Doppler echocardiographic findings in healthy Chinese adults.

To establish a norm for cardiac velocities in healthy Chinese adults, we examined 30 normal subjects (15 men and 15 women) with pulsed- and continuous-wave Doppler, and color flow mapping. The subjects ranged in age from 18 to 60 years (mean 37 years). We found that the early (E) and late (A) diastolic peak velocities for the mitral valve were 87 +/- 16 cm/sec and 61 +/- 15 cm/sec, respectively. The E/A ratio was 1.5 +/- 0.4. The E and A peak velocities for the tricuspid valve were 57 +/- 10 cm/sec and 40 +/- 7 cm/sec, respectively. The peak velocities for the left ventricular outflow tract, the ascending aorta, the proximal descending aorta and the main pulmonary artery were 77 +/- 19, 106 +/- 20, 96 +/- 24 and 74 +/- 17 cm/sec, respectively. None of the velocities exceeded 154 cm/sec. There were no significant differences between men and women. However, older subjects (greater than or equal to 40 years) had a higher mitral A velocity (69 +/- 13 cm/sec vs 57 +/- 17 cm/sec, p less than 0.05) and a lower E/A ratio (1.3 +/- 0.4 vs 1.6 +/- 0.3, p less than 0.05) than did subjects under 40 years of age. Mild tricuspid regurgitation was detected in 8 of the 30 subjects (27%), mitral regurgitation in 3 of the subjects (10%) and pulmonic regurgitation in one of the subjects (3%). There was no aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Doppler and two-dimensional echocardiographic features of sinus of Valsalva aneurysm.

Doppler, contrast, and two-dimensional echocardiograms of 12 aneurysms of the sinus of Valsalva in 10 consecutive patients were analyzed in order to highlight the diagnostic features. The diagnosis were confirmed by surgical and/or catheterization findings. The aneurysms had ruptured in 7 of 12 (58%). Two-dimensional echocardiography prior to the contrast studies was able to delineate the aneurysms in 7 of 12 (58%). The contrast studies outlined two additional aneurysms. The right aneurysms directed anteriorly and caudally. The noncoronary aneurysms formed an extraneous lumen at the posterior part of the aortic root, mimicking aortic dissection. Doppler examinations showed systolic and diastolic turbulence in five of six (83%) of the right aneurysms rupturing into the right ventricular outflow tract. Color Doppler echocardiography showed a left ventricular diastolic turbulence emanating from the aneurysm in a case with a noncoronary aneurysm rupturing into the left ventricle. It is concluded that the principal Doppler, contrast, and two-dimensional echocardiographic features usually allow a rapid correct diagnosis of sinus of Valsalva aneurysm.

Adult↗
PubMed1988

Cutaneous and pericardial extramedullary hematopoiesis with cardiac tamponade in chronic myeloid leukemia.

A 48-year-old woman with Philadelphia chromosome-positive chronic myeloid leukemia developed skin and pericardial extramedullary hematopoiesis. The echocardiogram revealed massive pericardial effusion with signs of tamponade. The cytocentrifuge preparation of pericardial fluid demonstrated all three hematopoietic components. Assays for the granulocyte-macrophage progenitor cells and erythroid progenitors on her pericardial fluid gave rise to colony numbers comparable to those of normal bone marrow cells. The patient was successfully treated with pericardiocentesis followed by short-term indwelling catheter drainage and administration of hydroxy-urea. There was no reaccumulation of fluid at ten months.

Cardiac Tamponade↗