Biomedical subjects

Cheuk-Man Yu

Publications and source records attributed to Cheuk-Man Yu.

47 records · Page 3Linked to original sources

PubMed2003

Comparison of acute changes in left ventricular volume, systolic and diastolic functions, and intraventricular synchronicity after biventricular and right ventricular pacing for heart failure.

BACKGROUND: Biventricular pacing (BiV) therapy has recently been shown to improve systolic function and cause reverse remodeling in patients with advanced heart failure with electromechanical delay. In these patients, the benefit of right ventricular (RV)-based pacing was controversial. We compared the acute changes in systolic and diastolic function, left ventricular (LV) volume, and intraventricular synchronicity in BiV pacing, RV pacing, and without pacing (No) by means of echocardiography and tissue Doppler imaging (TDI). METHODS: TDI was performed in 33 patients with heart failure after undergoing pacemaker implantation, when the device was randomized to BiV, RV, and no pacing modes. RESULTS: Systolic function was only improved during BiV pacing, but not during RV pacing. This included ejection fraction (No vs RV vs BiV = 24% +/- 12% vs 25% +/- 10% vs 30% +/- 14%, P =.02 vs No), +dp/dt (P =.01), myocardial performance index (P =.01), and isovolumic contraction time (P =.03). Mitral regurgitation was only reduced during BiV pacing (P =.02). LV early diastolic function was depressed in both RV and BiV pacing, as detected by transmitral flow (97 +/- 34 vs 80 +/- 34 vs 82 +/- 32 cm/s, both P < or =.005) and TDI (mean myocardial early diastolic velocity of 6 basal segments, 3.3 +/- 1.7 vs 2.6 +/- 1.0 vs 2.6 +/- 1.0 cm/s, both P =.01). The LV end-diastolic (187 +/- 86 vs 177 +/- 84 vs 166 +/- 79, P =.003) and end-systolic (146 +/- 77 vs 138 +/- 79 vs 122 +/- 69, P =.003) volumes were only decreased during BiV pacing. For systolic synchronicity, a significant delay in peak systolic contraction in the lateral over the septal wall (171 +/- 37 vs 217 +/- 46 ms, P =.004) was revealed by TDI when there was no pacing. This was abolished by BiV pacing, in which septal contraction was delayed (195 +/- 38 vs 201 +/- 53 ms, P = not significant). However, RV pacing restored the lateral wall delay, and systolic asynchrony reappeared (190 +/- 40 vs 227 +/- 56 ms, P =.01). Diastolic asynchrony between the septal and lateral walls was not evident in these patients and was not affected by either pacing mode. CONCLUSION: Only BiV pacing, but not RV pacing, improves systolic function, and reduces mitral regurgitation and LV volumes in patients with heart failure and electromechanical delay. This is attributed to the improvement of systolic synchronicity. Diastolic synchronicity was unaffected, whereas early diastolic function could be jeopardized, by either pacing mode.

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PubMed2003

Advances in devices for cardiac resynchronization in heart failure.

Patients with advanced heart failure have a high mortality and morbidity despite medical therapy. Depending on the underlying heart disease and severity of heart failure, 3.7 to 52.8% of patients have a QRS complex > or =120 ms who may have interventricular and intraventricular dyssynchrony correctible by cardiac resynchronization therapy (CRT). The latter is usually achieved with biventricular pacing, with the left ventricular lead placed in a tributary of the coronary sinus (CS), with a reported success rate between 88-92%. The technical advances for implantation include preformed guide sheaths to cannulate the CS, over the wire leads with passive fixation mechanism, and surgical placement methods. Device-specific CRT features include optimizing heart failure through insurance of a high percentage of pacing, heart failure monitoring, atrioventricular and interventricular timing, and avoiding double ventricular sensing. Furthermore, arrhythmic co-morbidities of heart failure such as atrial fibrillation and ventricular tachyarrhythmias can also be managed. Recent prospective trials suggest that there is a 30% reduction in heart failure hospitalization with CRT, and preliminary results suggest a survival benefit with CRT and implantable cardioverter defibrillator over optimal medical therapy.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2003

Regional left ventricle mechanical asynchrony in patients with heart disease and normal QRS duration: implication for biventricular pacing therapy.

LV electromechanical delay results in asynchronized contraction. However, it is not known if the presence of cardiac diseases without QRS prolongation may result in inter- or intraventricular asynchrony. This study investigated the occurrence of systolic mechanical delay in different regions of the LV in patients with underlying heart diseases and normal QRS duration. Tissue Doppler imaging (TDI) was performed in 141 patients (age 63.7 +/- 11.5 years) with underlying heart diseases (82% had ischemic heart disease) and 92 normal healthy volunteers (age 63.9 +/- 9.8 years) based on the four-basal and four-mid-segment model by apical views. Of these, 124 patients had normal QRS duration (< or = 120 ms) while 17 were prolonged due to LBBB or intraventricular conduction defect. Patients with normal QRS duration had significantly lower peak myocardial isovolumic contraction velocity (IVCM), sustained systolic velocity (SM), and prolonged time to peak IVCM and SM in almost all myocardial segments when compared to controls. The time to peak IVCM (basal lateral vs basal septal segment: 61.0 +/- 29.4 vs 53.3 +/- 24.1 ms, P < 0.005) and SM (basal lateral vs basal septal segment: 174 +/- 44 vs 154 +/- 36 ms, P < 0.001) was further delayed in the LV free-wall segments. Mechanical delay was also evident in the LV free-wall segments in patients with preserved or impaired systolic function, in patients with or without previous myocardial infarction, and in patients with prolonged QRS duration. Patients with prolonged QRS had a higher prevalence of LV free-wall delay of > 50 ms (47 vs 24%, chi-square = 4.6, P < 0.05). In conclusion, the presence of cardiac diseases was characterized by LV global mechanical delay; and, intraventricular asynchronized contraction characterized mostly by further mechanical delay in the free-wall region. These changes occur even in those with normal QRS duration.

Cardiac Pacing, Artificial↗

PubMed2003

Assessment of left and right ventricular systolic and diastolic synchronicity in normal subjects by tissue Doppler echocardiography and the effects of age and heart rate.

OBJECTIVES: This study examined inter- and intraventricular synchronicity in systole and diastole by tissue Doppler imaging (TDI), and investigated if these parameters and the regional velocities were affected by age and heart rate. METHODS: TDI was performed in 106 normal subjects (64.3 +/- 9.5 years, 60% male) using three apical views and a six-basal, six mid-segmental model. The regional parameters measured off line in both ventricles included peak isovolumic contraction velocity IVC(M), peak sustained systolic velocity (SM), peak early diastolic velocity (EM), peak late diastolic velocity (AM), and the E/AM ratio, as well as their time to these peak velocities: T(IVC), T(S), T(E), and T(A). RESULTS: The systole and diastole within the left ventricle (LV) was highly synchronized without difference in T (IVC), TS, TE, and TA. However, the right ventricle (RV) was about 20 msec later than the LV for T(IVC) and TS. For regional velocities, IVC(M), S(M), E(M), and A(M) were significantly higher in basal than mid-segments (all P < 0.001). In the base of the LV, SM, and EM were the highest at the lateral segment and the lowest at the anterolateral segment. Age and heart rate did not affect systolic velocities or the timing of events. In diastole, age correlated negatively with EM(r =-0.36 to -0.48, P <or= 0.001)and E/AM ratio(r =-0.37 to -0.51, P <or= 0.01), while increasing heart rate affected AM (r = 0.17 to 0.43) positively and TE(r =-0.49 to -0.66, P < 0.001)and TA(r =-0.85 to -0.93, P < 0.001)negatively. CONCLUSION: (1). Systolic and diastolic functions of the normal hearts are highly synchronized, though LV contraction slightly preceded that of RV. (2). Age and heart rate predominantly affect the diastolic, but not systolic, parameters that need to be taken into account.

Age Factors↗

PubMed2003

Expression of macrophage migration inhibitory factor in acute ischemic myocardial injury.

Macrophage migration inhibitory factor (MIF) is a key mediator in inflammatory or immune-mediated diseases, although its role in heart diseases is unknown. This study investigated the expression of MIF in the myocardium in the development of acute myocardial infarction (AMI). By use of immunohistochemistry, Western blotting, RT-PCR, and in situ hybridization, the gene and protein expression of MIF in the heart at 6 hr, 1 day, 3 days, 1 week, and 2 weeks after AMI was studied. In both normal and sham-operated rats, MIF mRNA and protein were expressed constitutively at low levels by the myocytes. By contrast, MIF mRNA was rapidly upregulated by the surviving myocytes in the infarcted region and, to a lesser extent, the non-infarcted region, accounting for a sevenfold increase at 6 hr after AMI (p<0.001). This was followed by a fourfold increase in MIF protein expression at day 1 after AMI (p<0.05). Macrophages were found accumulated in the infarcted region, being significant at day 1 (p<0.01) and progressive increased over the 2-week time course (p<0.01) in which MIF was found expressed in these cells. The results indicated that the infiltrating macrophages and myocytes were sources of MIF in the infarcted region. The latter cells became activated and involved in the amplification of inflammatory response in AMI. Therefore, upregulation of myocardial MIF may contribute to macrophage accumulation in the infarcted region and their pro-inflammatory role may participate in the myocyte damage seen in AMI.

Animals↗

PubMed2002

Progression of systolic abnormalities in patients with "isolated" diastolic heart failure and diastolic dysfunction.

BACKGROUND: The definition of diastolic heart failure (DHF) relies on the use of sensitive tools to exclude the presence of systolic dysfunction. The use of ejection fraction (EF) of 50% as the cutoff point may not be adequate to address such a task. We believe that systolic dysfunction is common in DHF. METHODS AND RESULTS: Echocardiography with tissue Doppler imaging was performed in 339 subjects, of whom 92 had systolic heart failure (SHF) (EF<50%), 73 had DHF (EF > or = 50% with diastolic abnormalities on Doppler echocardiography), and 68 had isolated diastolic dysfunction (DD); 106 were normal control subjects. Regional myocardial velocity curves were constructed off-line with the use of a 6-basal, 6-midsegmental model. The peak regional myocardial sustained systolic (S(M)) and early diastolic (E(M)) velocities were significantly lower in patients with SHF, DHF, and DD than in control subjects in almost all the myocardial segments. Likewise, the mean S(M) (SHF<DHF<DD<control subjects; 3.3 plus/minus 1.0 < 4.6 plus/minus 1.3 < 5.4 plus/minus 1.0 < 6.3 plus/minus 1.0 cm/s; all P less-than-or-equal 0.001) and mean E(M) (SHF=DHF<DD<control subjects; 3.6 plus/minus 1.2 =3.9 plus/minus 1.3 < 5.3 plus/minus 1.6 < 7.2 plus/minus 1.7 cm/s; all P<0.001) from the six basal segments were decreased in all the disease groups. A mean S(M) of 4.4 cm/s (-2 SD of control subjects) predicted the presence of systolic dysfunction in 92% of patients with SHF, 52% with DHF, and 14% with DD. CONCLUSIONS: Through the use of tissue Doppler imaging, systolic abnormalities were evident in patients previously labeled as DHF and to a much lesser extent, isolated DD. This indicates the common coexistence of systolic and diastolic dysfunction in a spectrum of different severity in the pathophysiological process of heart failure.

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PubMed2002

Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure.

BACKGROUND: Biventricular pacing has been proposed to improve symptoms and exercise capacity in patients with advanced heart failure and wide electrocardiographic wave complexes. This study investigated the effect of biventricular pacing on reverse remodeling and the underlying mechanisms. METHODS AND RESULTS: Twenty-five patients with NYHA class III to IV heart failure and electrocardiographic wave complex duration >140 ms receiving biventricular pacing therapy were assessed serially up to 3 months after pacing and when pacing was withheld for 4 weeks. Tissue Doppler echocardiography was performed using a 6-basal, 6-mid segmental model to assess the time to peak sustained systolic contraction (T(S)). There was significant improvement of ejection fraction, dP/dt, and myocardial performance index; decrease in mitral regurgitation, left ventricular (LV) end-diastolic (205+/-68 versus 168+/-67 mL, P<0.01) and end-systolic volume (162+/-54 versus 122+/-42 mL, P<0.01); and improved 6-minute hall-walk distance and quality of life score after pacing for 3 months. The mechanisms of benefits were as follows: (1) improved LV synchrony, as evident by homogeneous delay of T(S) to a timing close to the latest (usually the lateral) segment abolishing the intersegmental difference in T(S) and decreasing the standard deviation of T(S) within the left ventricle (37.7+/-10.9 versus 29.3+/-8.3 ms, P<0.05); (2) improved interventricular synchrony; and (3) shortened isovolumic contraction time (122+/-57 versus 82+/-36 ms, P<0.05) but increased diastolic filling time. These benefits are pacing dependent, because withholding the pacing resulted in varying speeds in the loss of cardiac improvements. CONCLUSIONS: Biventricular pacing reverses LV remodeling and improves cardiac function. Improvement of LV mechanical synchrony seems to be the predominant mechanism.

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PubMed2002

A new technique for the transvenous implantation of the over-the-wire left ventricular pacing lead in a patient with heart failure.

Implantation of left ventricular leads (LV) for biventricular pacing remains a technological challenge and failure of the procedure is not uncommon. We described a 58 year-old patient with heart failure and intraventricular conduction delay where difficulty is encountered when cannulating the coronary sinus by the guiding catheter. By placing a guiding catheter in the inferior portion of the right atrium, a coronary guidewire, preloaded with an over-the-wire lead system, was used to reach the lateral cardiac vein. This may help to reduce the implant failure rate and avoid other more invasive means of LV lead implantation.

Cardiac Catheterization↗

PubMed2002

Effects of losartan and atenolol on left ventricular mass and neurohormonal profile in patients with essential hypertension and left ventricular hypertrophy.

OBJECTIVE: To compare the effects of the angiotensin II antagonist, losartan, with those of atenolol on left ventricular hypertrophy (LVH), blood pressure and neurohormone concentrations in hypertensive patients with LVH. DESIGN: A multinational, randomized, double-blind trial. SETTING: Hospital. PATIENTS: Hypertensive patients with an echocardiographically documented left ventricular mass index (LVMI) 120 g/m(2) (men) or 105 g/m(2) (women). INTERVENTIONS: Patients allocated randomly to groups received either losartan or atenolol 50 mg/day for 36 weeks, with possible titration to 100 mg/day, and addition of hydrochlorothiazide 12.5 or 25 mg/day. MAIN OUTCOME MEASURES: Changes in LVMI and sitting systolic (SBP) and diastolic (DBP) blood pressures after 36 weeks of treatment (study powered for non-inferiority hypothesis). All echocardiographic data were read in a central laboratory by staff blinded to the treatments and sequence of echocardiographic tapes. RESULTS: The estimated treatment difference between the losartan and atenolol regimens (mean change from baseline at week 36) in LVMI was -2.5 g/m(2) [95% confidence interval (CI) -7.36 to 2.37 g/m(2) ] in favor of losartan, indicating that losartan was significantly non-inferior ( 0.001, non-inferiority limit 8 g/m(2) ) and numerically superior to atenolol in reducing LVMI. The losartan-based regimen significantly reduced LVMI after 36 weeks compared with baseline (-6.56 g/m(2) , 95% CI -10.24 to -2.88 g/m(2) , P<0.001), whereas the atenolol-based regimen had no significant effect (-3.71 g/m, 95% CI -7.75 to 0.32 g/m(2) , P= NS). In a subset of 82 patients, significant changes in serum concentrations of atrial natriuretic peptide, brain natriuretic peptide and immunoreactive amino-terminal pro-brain natriuretic peptide were recorded in losartan-treated ( 0.01) but not atenolol-treated patients. Losartan and atenolol significantly decreased SBP and DBP from baseline after 6, 12, 24 and 36 weeks. The changes from baseline in DBP were greater in the atenolol group at weeks 6 and 36 [difference -2.6 mmHg ( P= 0.016) at week 36]. However, both treatment regimens achieved similar SBP/DBP values at week 36 (141.1 +/- 12.8/86.8 +/- 8.2 mmHg for losartan and 141.4 +/- 17.2/85.0 +/- 10.1 mmHg for atenolol, respectively). Overall, losartan treatment was associated with significantly fewer drug-related clinical adverse events, compared with atenolol (10 and 22%, respectively, P= 0.028). CONCLUSIONS: Both losartan- and atenolol-based regimens effectively decreased blood pressure. Losartan was non-inferior and numerically superior to atenolol in regression of LVH. The reduction in hypertrophy with losartan treatment was accompanied by reductions in circulating concentrations of cardiac natriuretic peptides. Losartan, by specifically blocking angiotensin II, may therefore have effects on the heart beyond those expected from the decrease in blood pressure alone. Losartan was better tolerated than atenolol.

Aged↗

PubMed2002

Stable and optimal anticoagulation is achieved with a single dose of intravenous enoxaparin in patients undergoing percutaneous coronary intervention.

This study assessed the pharmacokinetics, safety and efficacy of intravenous enoxaparin in patients undergoing percutaneous coronary intervention (PCI). Sixty consecutive patients [(age, 62 11 years; female, 16%; diabetes, 18%; hypertension, 53%; prior myocardial infarction (MI), 43%] undergoing PCI (stable angina, 89%; stent, 92%; two-vessel disease, 23%; B2/C lesions, 45%) were administered intravenous enoxaparin 1 mg/kg for procedural anticoagulation. Blood samples for anti-Xa level and activated partial thromboplastin time (aPTT) were assayed from the first 20 patients before and after enoxaparin administration at the following intervals: 5, 30, 60, 90, 120, 150, 180, 210, 240, 360 and 480 minutes. Activated clotting time was assessed 5 minutes after enoxaparin administration. Bleeding complications were classified according to Thrombolysis In Myocardial Infarction (TIMI) criteria. All patients were monitored for adverse clinical events at clinic visit 4 8 weeks after hospital discharge. No TIMI major or minor bleedings occurred during hospitalization for the PCI (median stay post-PCI = 1 day). One patient (2%) developed a non-Q wave MI after the PCI and before hospital discharge. There was no death or urgent revascularization up to clinical follow-up. The peak anti-Xa level was 1.30 0.18 IU/ml (range, 1.03 1.69 IU/ml). The minimum anti-Xa level was 0.55 IU/ml 4 hours after enoxaparin. Thus, the use of intravenous enoxaparin in patients undergoing PCI is associated with a low incidence of ischemic and bleeding complications. A stable therapeutic anticoagulant effect is provided without the need for monitoring within 4 hours of enoxaparin administration.

Aged↗

PubMedDate not supplied

New insight into left ventricular reverse remodeling after biventricular pacing therapy for heart failure.

Biventricular pacing has been consistently shown to improve symptoms and exercise capacity in patients with advanced heart failure and wide QRS complexes. Recent data have shown that biventricular pacing has the propensity to reduce left ventricular volume, a condition referred to as reverse remodeling. Since the authors initial description of successful left ventricular reverse remodeling after biventricular pacing therapy, data from multicenter trials have grown and consistently support the observation. In addition to the volumetric change, there was also progressive improvement of left ventricular systolic function and clinical status. The authors subsequent data also illustrated that the benefits on reverse remodeling and left ventricular systolic function were pacing dependent and disappeared gradually when pacing was withdrawn. With the use of tissue Doppler imaging, a substantial proportion of patients were found who had mechanical delay in the free wall. During biventricular pacing, all the segments were homogenously delayed resulting in a late, albeit synchronous, systolic contraction.

Cardiac Pacing, Artificial↗