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Biomedical subjects

C P Lau

Publications and source records attributed to C P Lau.

At least 19 recordsLinked to original sources
PubMed2001

Plasma nitric oxide level in heart failure secondary to left ventricular diastolic dysfunction.

Nitric oxide (NO) is a free radical that is elevated in the plasma of patients with systolic heart failure. However, its relation to diastolic function is unknown. This study investigated the relation between the level of stable end-products of plasma NO (NOx level) and diastolic function in patients with heart failure. We performed echocardiographic Doppler studies in 76 patients (mean age of 66 +/- 10 years, 75% men) with congestive heart failure. Left ventricular (LV) diastolic dysfunction was classified as either a restrictive (RFP) or nonrestrictive filling pattern (non-RFP). Same day venous total nitrite plus nitrate levels were measured by chemiluminscence. Both patients with isolated diastolic heart failure (ejection fraction >50%) (77 +/- 9 micromol/L, n = 33) and systolic failure (ejection fraction < or = 50%) (115 +/- 17 micromol/L, n = 43) had significantly higher plasma NOx levels than controls (37 +/- 2 micromol/L, both p <0.001). RFP coexists mostly in patients with systolic heart failure (15 of 18), and these patients had a higher NOx level than patients with systolic failure and a non-RFP (n = 28) (163 +/- 35 vs 88 +/- 16 micromol/L, p <0.05). Patients who were not on oral nitrate drugs had insignificant lower plasma NOx levels than those on regular nitrate therapy, although it was still higher than controls. Plasma NOx level did not correlate with LV ejection fraction. Stepwise multiple regression analysis confirmed that the presence of RFP was the only independent predictor of NOx, and hence NO production. Plasma NOx level is elevated in patients with isolated diastolic heart failure. In addition, in patients with LV systolic failure, the severity of LV diastolic dysfunction determines the amount of NO production.

Aged↗
PubMed2001

Dual-site atrial pacing for atrial fibrillation in patients without bradycardia.

Atrial pacing has been shown to delay the onset of atrial fibrillation (AF) when compared with ventricular pacing in patients with sick sinus syndrome. The role for pacing in the control of AF in patients without bradycardia is uncertain. We performed a randomized, crossover, single-blinded study in 22 patients (14 women, aged 63 +/- 10 years) with paroxysmal AF refractory to treatment with oral sotalol (202 +/- 68 mg/day) and no bradycardic indication for pacing. All patients received a dual-chamber pacemaker with 2 atrial pacing leads positioned at the high right atrium and coronary sinus ostium, respectively. Patients were randomized in a crossover fashion to be paced for 12 weeks, either with high right atrial (RA) pacing at 30 beats/min ("Off") or dual-site RA pacing with an overdrive algorithm that maintained atrial pacing at a rate slightly above the sinus rate ("On"). Treatment on resulted in a significantly higher percentage of atrial pacing and a reduction in atrial ectopic frequency than the treatment off period. The time to the first clinical AF recurrence was prolonged (15 +/- 17 to 50 +/- 35 days, p = 0.006), and total AF burden was reduced (45 +/- 34% vs 22 +/- 29%, p = 0.04) in the on-treatment phase. However, there was no difference in AF checklist symptom scores or overall quality-of-life measures. Dual-site RA pacing with continued sinus overdrive prolonged the time to AF recurrence and decreased AF burden in patients with paroxysmal AF. The absence of a major impact on symptom control suggests that pacing should be used as an adjunctive therapy with other treatment modalities for AF.

Adolescent↗
PubMed2001

Effect of verapamil on prevention of atrial fibrillation in patients implanted with an implantable atrial defibrillator.

BACKGROUND: The role of verapamil in the prevention of atrial fibrillation (AF) in patients with recurrent AF is unknown. HYPOTHESIS: The aim of this study was to evaluate the effect of verapamil on the prevention of AF in patients implanted with an implantable atrial defibrillator (IAD). METHODS: The effects of verapamil (240 mg/day) on the total duration of AF, number of AF recurrences, and number of cardioversions were prospectively evaluated in a randomized, crossover fashion over an 8-week period in 11 patients (9 men, 2 women; mean age: 60 +/- 6 years) implanted with an IAD. RESULTS: Implantable atrial defibrillators successfully converted 13 of 14 (93%) spontaneous episodes of AF. There was no significant difference in the efficacy of cardioversion (86 vs. 100%, p = 0.8), the total duration of AF (173 +/- 198 vs. 270 +/- 241 h, p = 0.5), the number of AF episodes (8.5 +/- 9.0 vs. 9.3 +/- 10.2, p = 0.3), and the number of cardioversions (1.7 +/- 2.4 vs. 1.8 +/- 2.1 p = 0.7) with or without treatment with verapamil. CONCLUSIONS: The results of the present study suggest that treatment with verapamil has no significant effect on the prevention of AF in patients treated with an LAD.

Anti-Arrhythmia Agents↗
PubMed2001

Should all implantable cardioverter defibrillators for ventricular arrhythmias be dual-chamber devices?

The advantages of a dual-chamber implantable cardioverter defibrillator (ICD) over a single-chamber ICD include physiologic pacing capability, atrial electrogram storage, enhanced arrhythmia discrimination algorithms, and a potential to treat atrial arrhythmia by pacing or defibrillation. Current evidence supports the supposition that dual-chamber ICDs are definitely indicated in patients who have a concomitant indication for physiologic pacing, such as bradycardia or bradycardia-dependent ventricular tachyarrhythmias. Refined dual-chamber arrhythmia discrimination algorithms and enhanced atrial therapies are probably required for patients with frequent supraventricular arrhythmias. Furthermore, in patients with systolic heart failure, low ejection fraction, and intraventricular conduction delay, triple-chamber ICDs with biventricular pacing may improve their functional status and prevent sudden arrhythmic death. Careful patient selection is required to optimize the cost-effectiveness of these sophisticated technologies.

Arrhythmias, Cardiac↗
PubMed2001

Effects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarction.

OBJECTIVES: The goal of this study was to compare the relative efficacy of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin receptor blocker (ARB) in suppressing the histopathologic changes that lead to ventricular remodeling after an acute myocardial infarction (AMI). BACKGROUND: Myocardial interstitial fibrosis in the noninfarcted region is a major histologic landmark resulting in cardiac dysfunction after AMI. However, the relative potency of an ACE inhibitor and ARB on suppressing the histopathologic changes was unclear. METHODS: Rats with AMI were randomized to fosinopril, valsartan or a combination of the two drugs for two or four weeks. The total, type I and type III collagen and activated fibroblasts and macrophages were quantified by histomorphometry. The expression of transforming growth factor-beta 1 (TGF-beta 1) messenger ribonucleic acid (mRNA) was determined by reverse transcription polymerase chain reaction. RESULTS: Acute myocardial infarction resulted in significant elevation of total (p < 0.001) and type I (p < 0.001) collagen and a twofold increase in TGF-beta 1 mRNA expression (p < 0.001) in the septum at two and four weeks. Macrophages and activated myofibroblasts infiltrated extensively in the infarct zone. Treatment with valsartan or combination therapy normalized the total and type I collagen (p < 0.001) as well as TGF-beta 1 mRNA level (p < 0.01) in the septum and was associated with the suppression of macrophages and myofibroblasts in the infarct zone (p < 0.01). Fosinopril was less effective than valsartan or combination therapy. CONCLUSIONS: The use of valsartan, especially combined with fosinopril, was more effective than fosinopril in the suppression of histopathologic changes resulting in cardiac remodeling after AMI. This study has important therapeutic implications in pharmacotherapy of clinical practice.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

P wave polarity during pacing in pulmonary veins.

INTRODUCTION: Recent studies have demonstrated that premature depolarizations that trigger atrial fibrillation often arise in pulmonary veins. The purpose of this study was to evaluate whether P wave polarity is helpful in distinguishing which of the 4 pulmonary veins is the site of origin of a premature depolarization. METHODS AND RESULTS: In 28 patients without structural heart disease who underwent focal ablation of paroxysmal atrial fibrillation, P wave polarity on a 12-lead electrocardiogram (ECG) was analyzed during sinus rhythm, and during pacing at a cycle length of 500--600 ms in the high right atrium and within each of the 4 pulmonary veins. P waves were categorized as positive, negative, biphasic or isoelectric. A negative or biphasic P wave in lead I (sensitivity 85 %, specificity 71 %) or a positive P wave in V1 (sensitivity 85 %, specificity 89 %) were helpful in predicting a pulmonary venous site of origin as opposed to a right atrial site of origin. A positive P wave in lead II and III distinguished superior from inferior pulmonary veins (sensitivity 90 %, specificity 84 %). The sensitivity and specificity of negative or biphasic P waves in lead aVL in distinguishing a left from right pulmonary vein site of origin were 94 % and 42 %, respectively. CONCLUSIONS: Analysis of P waves polarity may be helpful in localizing the pulmonary vein that is the site of origin of a premature depolarization. Among the 12 ECG leads, I, II, III, aVL, and V1 are the most helpful in regionalizing premature depolarizations arising in the pulmonary veins.

Adult↗
PubMed2001

A cephalic vein cutdown and venography technique to facilitate pacemaker and defibrillator lead implantation.

The aim of this study was to assess the feasibility of a cephalic vein cutdown and venography technique for implantation of a pacemaker or ICD and to determine the causes of failure of cephalic vein cutdown. In consecutive patients who underwent pacemaker or ICD implants, a modified cephalic vein guidewire technique was performed. This technique was attempted in 289 pacemaker implants and 26 ICD implants (155 men, 160 women; mean age 74 +/- 10 years). The success rate for implantation of a single chamber and a dual chamber device by using this technique alone was 84% (54/64) and 74% (185/251), respectively (P = 0.10). In an additional 7% of patients with dual chamber implant, the cephalic vein can be used for passage of the ventricular lead. A cephalic venogram was required in 82 patients and facilitated the passage of the guidewire in 62 (79%) of them. No complication related to vascular access was observed with this technique. This technique failed in 54 (17%) of 315 patients due to (1) failure of cephalic vein isolation (48%), (2) venous stenosis (24%), or (3) venous torturosity or anomalies (28%). There were no significant differences in the patient's age, sex, type of device, and the fluoroscopic time for lead placement between patients with or without successful lead placement using this technique (all P > 0.05). In conclusion, a simple modification of the cephalic vein guidewire technique together with venography has facilitated the placement of leads during pacemaker and ICD implant. This technique is safe and applicable in the majority of patients and avoids the risk of subclavian puncture.

Adult↗
PubMed2001

Reversible impairment of left and right ventricular systolic and diastolic function during short-lasting atrial fibrillation in patients with an implantable atrial defibrillator: a tissue Doppler imaging study.

AF with a fast ventricular response may cause ventricular mechanical impairment, though whether short-lasting AF with satisfactory rate control may affect ventricular function is unknown. This study investigated if prompt cardioversion by an implantable atrial defibrillator (IAD) may prevent left (LV) and right ventricular (RV) systolic and diastolic dysfunction. Ten patients (mean age 61 +/- 9 years, 8 men) with paroxysmal AF without structural heart disease who received an IAD were studied by echocardiography and tissue Doppler imaging (TDI) for both ventricles. Measurements were made during baseline sinus rhythm and at 1-minute, 20-minute, 4-hour, and 1-week postcardioversion of an episode of spontaneous AF. The occurrence of AF and the ventricular rate were monitored at 2-hour intervals by the device. There were 50 episodes of AF with a mean duration of 8.8 +/- 8.9 days (2 hours to 37 days). There was no difference in M-mode measured LV fractional shortening and ejection fraction between baseline sinus rhythm and after cardioversion. However, the TDI derived myocardial systolic velocity (TDI-S) was significantly lower at 1-minute postcardioversion and was normalized at 1 week in both LVs (baseline: 5.7 +/- 1.8, 1 minute: 4.2 +/- 1.0, 20 minutes: 4.3 +/- 0.9, 4 hours: 4.8 +/- 1.0, 1 week: 5.5 +/- 1.8 cm/s; P < 0.005 when comparing 1 minute and 20 minutes to baseline; P < 0.05 when comparing 4 hour to baseline) and RV (baseline: 10.4 +/- 2.1, 1 minute: 7.8 +/- 1.4, 20 minutes: 8.1 +/- 1.2, 4 hours: 9.2 +/- 1.5, 1 week: 10.0 +/- 2.0 cm/s; P < 0.005 when comparing 1 minute, 20 minutes, and 4 hours to baseline). For diastolic function, transmitral Doppler study showed a decrease in early filling velocity at 1 minute (P < 0.05) and 20 minutes (P < 0.005), which was normalized at 4 hours. There was no change in transtricuspid Doppler flow. However, TDI derived myocardial early filling velocity was decreased in the LV (baseline: 6.0 +/- 2.8, 1 minute: 5.4 +/- 2.3, 20 minutes: 5.4 +/- 2.1, 4 hours: 6.1 +/- 2.2, 1 week: 5.8 +/- 1.7 cm/s; P < 0.05 when comparing 1 minute and 20 minutes to baseline) and RV (baseline: 8.9 +/- 3.5, 1 minute: 7.9 +/- 3.3, 20 minutes: 8.1 +/- 3.3, 4 hours: 8.5 +/- 2.9, 1 week: 8.4 +/- 3.5 cm/s; P < 0.05 when comparing 1 minute to baseline). AF of a longer duration (> 48 hours) resulted in a more depressed TDI-S in LV (> 48 hours: 4.2 +/- 1.0, < or = 48 hours: 5.3 +/- 1.3 cm/s; P < 0.01). Shocks in sinus rhythm did not affect any of the above echocardiographic parameters. Therefore, despite adequate rate control, short-lasting AF impairs systolic and diastolic function in both ventricles, which improves gradually after cardioversion. Early restoration of sinus rhythm by an IAD minimizes ventricular dysfunction. TDI is a sensitive tool to assess early systolic and diastolic dysfunction.

Atrial Fibrillation↗
PubMed2001

Increase in plasma adrenomedullin in patients with heart failure characterised by diastolic dysfunction.

OBJECTIVE: To investigate the relation between plasma adrenomedullin and the severity of diastolic dysfunction in patients with heart failure. DESIGN: Prospective study. SETTING: University teaching hospital. PATIENTS: 77 patients (mean (SEM) age 66.3 (1.2) years; 75% male) who were being followed in the outpatient clinic after admission to hospital for acute heart failure. INTERVENTIONS: Same day echocardiography with Doppler studies; determination of venous adrenomedullin concentration by radioimmunoassay. MAIN OUTCOME MEASURES: Plasma adrenomedullin concentration and its correlation with systolic and diastolic function. RESULTS: 31 patients (40%) had isolated diastolic dysfunction (ejection fraction > 50%), and the remaining 46 had a depressed ejection fraction (< 50%). Of the patients with diastolic dysfunction, 17 had a restrictive filling pattern. In all but one of these there was coexisting systolic failure (chi(2) = 10.7, p = 0.001). Patients with systolic heart failure and a restrictive filling pattern (group 1, n = 16) had a higher plasma adrenomedullin than those with systolic failure and a non-restrictive filling pattern (group 2, n = 30) or with isolated diastolic heart failure and a non-restrictive filling pattern (group 3, n = 30) (mean (SEM): 91.7 (21.1) v 38.4 (8.8) v 34.0 (6.5) pmol/l, both p < 0.05). All heart failure values were higher (p < 0.01) than the control value (6.9 (1.2) pmol/l). Ejection fraction and left ventricular dimensions were similar in groups 1 and 2. Plasma adrenomedullin did not correlate with ejection fraction or New York Heart Association functional class. Stepwise multiple regression analysis showed that the presence of a restrictive filling pattern was the only independent variable associated with a high plasma adrenomedullin. CONCLUSIONS: Plasma adrenomedullin concentrations in patients with heart failure are determined by the presence of diastolic dysfunction, and are especially raised in the presence of a restrictive filling pattern. There appears to be no correlation with systolic dysfunction.

Acute Disease↗
PubMed2001

Evaluation of CYP2D6 oxidation of dextromethorphan and propafenone in a Chinese population with atrial fibrillation.

The objective of this study was to determine the percentage of patients with paroxysmal atrial fibrillation who were poor metabolizers of CYP2D6 in a Chinese population from Hong Kong and to assess the relationship between the dextromethorphan/dextrorphan ratio and the propafenone/5-hydroxypropafenone ratio or the steady-state propafenone concentration. Patients (n = 60) were recruited from the Arrhythmia Clinic at the University of Hong Kong and given dextromethorphan 30 mg. The dextromethorphan and dextrorphan concentrations in urine over the next 8 hours were used to determine metabolizer status. If the metabolic ratio was greater than 0.3, the patient was determined to be a poor metabolizer. In phase 2, patients (n = 38) were given propafenone 150 mg twice daily, and at steady state, the propafenone and 5-OH propafenone plasma concentrations were determined. It was found that 15% of the patients were poor metabolizers of dextromethorphan. There was a significant correlation between the metabolic ratios of dextromethorphan/dextrorphan and propafenone/5-OH propafenone (r = 0.49, p = 0.0019) and between the dextromethorphan/dextrorphan ratio and the concentration of propafenone (r = 0.32, p = 0.05). No correlations were found in the extensive or poor metabolizer subgroups. It was concluded that the percentage of poor metabolizers in atrial fibrillation patients from Hong Kong was much larger than in previous studies of Chinese patients who were not from Hong Kong. The ability to metabolize dextromethorphan to dextrorphan is related to the ability to metabolize propafenone to 5-hydroxypropafenone.

Anti-Arrhythmia Agents↗
PubMed2001

Antioxidative glucosides from the fruits of Ligustrum lucidum.

The ethanol extract of the fruits of Ligustrum lucidum was shown to have inhibitory effects on the hemolysis of red blood cells induced by 2,2'-azo-bis-(2-amidinopropane) dihydrochloride. Bioassay-guided analysis led to the isolation of ten secoiridoid glucosides. Two of them were new, lucidumosides C and D. Their structures were elucidated by spectroscopic methods. The other eight compounds were identified as oleoside dimethyl ester, ligustroside, oleuropein, nuezhenide, isonuezhenide, neonuezhenide, lucidumoside A and lucidumoside B. Five compounds, oleoside dimethyl ester, oleuropein, neonuezhenide, lucidumoside B and lucidumoside C, exhibited strong antioxidant effect against hemolysis of red blood cells induced by free radicals.

Antioxidants↗
PubMed2001

Continuous calcium chloride infusion for massive nifedipine overdose.

A 37-year-old woman presented with persistent hypotension and noncardiogenic pulmonary edema after massive nifedipine overdose. Judicious use of continuous and prolonged high-dose IV calcium infusion was administered to provide sustained increases in serum ionic calcium level (approximately 2 mmol/L) and was able to improve the hemodynamic status without any major adverse reaction.

Adult↗
PubMed2000

Control of paroxysmal atrial fibrillation recurrence using combined administration of propafenone and quinidine.

The frequent recurrence of paroxysmal atrial fibrillation (PAF) despite the use of standard antiarrhythmic agents prompted the use of new therapeutic approaches. There are few data on systematic assessment of PAF control with stepwise dose escalation and the use of a drug combination. Low-dose quinidine may promote the efficacy of propafenone by inhibiting its degradation through the cytochrome P450 pathway (CYP2D6). We prescribed propafenone 300 to 450 mg/day to 60 patients with PAF for 8 weeks, and 62% were symptomatically controlled. The 19 refractory patients were randomized in a double-blinded fashion to receive either a higher dose of propafenone (450 to 675 mg/day) or the standard dose of propafenone with low-dose quinidine 150 mg/day, each for an 8-week study period, and subsequently crossed over to the alternative treatment. The resulting serum propafenone concentrations were 259 +/- 208 and 336 +/- 237 mg/day (p >0.5), respectively. Both treatment arms prolonged the time to the first symptomatic atrial fibrillation (AF) recurrence and the interval between attacks, and AF was controlled in 37% of patients. However, the higher dose of propafenone was associated with gastrointestinal side effects not present with the low-dose quinidine combination. Of the 10 refractory patients, 7 were further controlled with a standard dose of propafenone plus quinidine (600 mg/day). Overall, control of PAF was achieved in 85% of patients at the end of 8 months; adverse effects necessitating withdrawal were observed in 6%, and uncontrolled AF in 5% of patients. There was no difference in the mean AF rate during recurrences in all phases, and ventricular proarrhythmia was not seen. This study documents the role of stepwise antiarrhythmic treatment of PAF. The use of a standard dose of propafenone, followed by low-dose quinidine combination to reduce propafenone degradation, and the combined standard dose of propafenone and quinidine may be used to maximize efficacy and tolerability.

Adolescent↗
PubMed2000

De novo expression of macrophage migration inhibitory factor in atherogenesis in rabbits.

Macrophage migration inhibitory factor (MIF) has been shown to play an important role in macrophage-mediated diseases. We investigate the potential role of MIF in atherogenesis using a hypercholesterolemic rabbit model. New Zealand White rabbits fed with a 2% cholesterol diet developed hypercholesterolemia and early fatty streaks at 1 month. The lesions became advanced at 3 months and were associated with de novo MIF expression by vascular endothelial cells (VECs) and smooth muscle cells (SMCs), as demonstrated by immunohistochemistry, reverse transcriptase-polymerase chain reaction, and in situ hybridization. By contrast, there was no increase in MIF levels in rabbits fed a normal diet. In early atherogenesis, marked upregulation of MIF mRNA and protein by VECs and some intimal cells were closely associated with CD68(+) monocyte adhesion onto and subsequent migration into subendothelial space. Of significance, the accumulation of macrophages was exclusively localized to areas of strong MIF expression, which may be associated with the macrophage-rich fatty streak lesion formation. Upregulation of MIF by SMCs is transient during atherogenesis. Importantly, strong MIF expression by activated macrophages may be responsible for the development of foam cell-rich lesions. Finally, the ability of MIF to induce intercellular adhesion molecule-1 expression by VECs implicates its pathogenic role in atherogenesis. In conclusion, the present study provides the first demonstration that MIF is markedly upregulated during atherogenesis. Upregulation of MIF by VECs and SMCs may play a role in macrophage adhesion, transendothelial migration, accumulation, and, importantly, transformation into foam cells. Furthermore, strong MIF expression by macrophages may both initiate and amplify the atherogenesis process.

Animals↗