Han B. Xiao

Impairment of autonomic reactivity is a feature of heart failure whether or not the left ventricular ejection fraction is normal

BACKGROUND Autonomic dysfunction (AD) is associated with morbidity and mortality in patients with systolic heart failure (SHF). The extent of AD when LV ejection fraction is preserved (HF-NEF), is unclear. Our objectives were: 1) quantitative assessment of autonomic function in SHF and HF-NEF; and 2) exploration of relationships among AD, symptoms and cardiac function. METHODS This was an observational study of patients newly referred from primary care with a heart failure diagnosis; 21 SHF, 20 HF-NEF patients and 21 normal subjects were recruited. All subjects underwent clinical evaluation, 6-minute walk test (6 MWT), Minnesota Questionnaire (MLWHFQ) and echocardiography. Autonomic assessment included haemodynamic responses to standing, deep breathing and handgrip. Concomitant blood pressure variability (BPV) and heart rate variability (HRV) parameters were also derived. RESULTS There were significant differences in all haemodynamic responses between SHF, HF-NEF and normal. Log transformed (ln) low frequency spectral component of BPV was lower in SHF (4.1 ± 0.3) than HF-NEF (4.2 ± 0.4) and normal (4.4 ± 0.1; p=0.001 SHF vs HF-NEF and vs normal). Ln LF/HF was greater in normal than HF-NEF and SHF (1.5 ± 0.7 vs 0.9 ± 1.0 vs 0.6 ± 0.6; p=0.003). Autonomic modulations correlated negatively with severity of heart failure. CONCLUSIONS Autonomic responses in heart failure were blunted and the attenuation of responses correlated strongly with symptomatic and functional markers of disease severity. Autonomic dysfunction is a feature of the heart failure syndrome but is not dependent on ejection fraction.

Induced ischemia detected by dobutamine stress echocardiography in coronary heart disease patients after myocardial re-vascularization.: Experience in a District General Hospital

Most episodes of myocardial ischemia in patients with known coronary artery disease (CHD) are asymptomatic. Silent myocardial ischemia (SMI) is an important predictor of adverse outcome in patients with proven coronary artery disease. beta-blockers are effective in suppressing ischemia, and improve clinical outcome in patients with coronary artery disease. At present, it is common practice to stop treatment with beta-blockers in clinically asymptomatic patients after coronary artery bypass graft (CABG) and/or myocardial re-vascularization (PTCA/Stent), although the possible presence of SMI/inducible ischemia after myocardial re-vascularization is not known. We examined 56 asymptomatic CHD patients after coronary artery bypass graft (n=36), percutaneous coronary angioplasty PTCA/stent (n=15), or both (n=5); therapy with beta-blockers was stopped in all of them after myocardial revascularization. All these patients underwent a dobutamine stress echocardiography test (DSE test). The DSE test was proposed to these asymptomatic CHD patients to investigate the possible presence of SMI/inducible ischemia after myocardial re-vascularization. All patients had history of myocardial infarction or evidence of mildly impaired left ventricular function at rest as assessed by cardiac catheterization. Abnormal DSE studies occurred in eight of the 56 patients (14%; 95% C.I.: 6-26%). Therapeutic approaches specifically targeted at reducing total ischaemic burden include pharmacologic therapy and myocardial revascularization. On the basis of these data, it can be concluded that asymptomatic CHD patients after myocardial re-vascularization must be re-evaluated to rule out SMI/inducible ischemia that can be treated (e.g. with beta-blockers) reducing cardiovascular morbidity and mortality.

Electrocardiographic associations of right precordial Q waves help to distinguish anterior myocardial infarction from aortic stenosis

Right precordial Q waves are ECG evidence of anterior myocardial infarction and can be present in patients with pathological left ventricular hypertrophy particularly caused by aortic stenosis. The aim of this study was to investigate the ECG features associated with Q waves in aortic stenosis and those in anterior myocardial infarction. We studied 16 patients with anterior myocardial infarction and 19 patients with aortic stenosis by means of ECG, echocardiography and clinical history. On the ECG, heart rate (70 +/- 20 beats/min vs. 83 +/- 20) and QT interval (380 +/- 65 ms vs. 390 +/- 50) did not differ between the two conditions. PR interval (160 +/- 15 ms vs. 185 +/- 30, P<0.05) and QRS duration (80 +/- 7.0 ms vs. 95 +/- 15, P<0.01) were both longer in patients with aortic stenosis than in those with myocardial infarction. The Q wave voltage in V1 (1.0 +/- 0.55 mV vs. 1.5 +/- 0.60) or V2 (1.3 +/- 0.5 mV vs. 1.8 +/- 0.85) and R wave voltage in V5 (0.7 +/- 0.7 mV vs. 2.1 +/- 0.9) or V6 (0.7 +/- 0.4 mV vs. 1.5 +/- 0.7, all P<0.01) were significantly less in patients with anterior myocardial infarction than in those with aortic stenosis. Q wave voltage over 1.3 mV in V1 or R wave voltage over 1.5 mV in V5 can differentiate aortic stenosis from anterior myocardial infarction with a sensitivity of 79% for each and specificities of 81 and 93.8%, respectively. Though the frontal QRS axis was similar in the two groups (28 +/- 45 degrees vs. 14 +/- 35, P>0.05), the horizontal QRS axis pointed laterally (-30 +/- 20 degrees) in aortic stenosis and posteriorly (-60 +/- 20 degrees, P<0.01) in anterior myocardial infarction. A horizontal QRS axis between zero and -45 degrees detected the presence of aortic stenosis with a sensitivity of 94.7% and a specificity of 81.3%. On echocardiography, left ventricular hypertrophy was found in most patients (94.7%) with aortic stenosis but not in those (0%) with anterior myocardial infarction. Left ventricular end diastolic dimensions (5.1 +/- 0.7 cm vs. 5.1 +/- 0.9, P>0.05) were similar in the two groups but the end systolic dimension was increased in patients with aortic stenosis (4.0 +/- 0.9 cm vs. 3.4 +/- 0.6, P<0.05). The systolic left ventricular function (shortening fraction: 23 +/- 8.0% vs. 34 +/- 7.0; Vcf: 0.8 +/- 0.26 circ/s vs. 1.3 +/- 0.26, both P<0.01) was significantly impaired in patients with aortic stenosis compared to those with myocardial infarction. In conclusion, in the presence of right precordial Q waves, the simple 12-lead ECG can provide important information on distinguishing anterior myocardial infarction from aortic stenosis. In particular, the QRS voltage in the chest leads and horizontal QRS axis can differentiate anterior myocardial infarction from aortic stenosis with high sensitivity and specificity.

Absent right precordial R waves are associated with reduced left ventricular function and poor prognosis in patients with aortic stenosis.

Right precordial Q waves can be present in patients with aortic stenosis as well as in those with anterior myocardial infarction. In order to evaluate the relationship of right precordial Q waves to left ventricular function and prognosis in patients with aortic stenosis, we studied 49 such patients with no history of myocardial infarction, by means of ECG, clinical history and echocardiography. 15 (31%) patients had Q waves in both V1 and V2 and 34 (69%) did not. There were no differences in age (77+/-9.0 years vs. 78+/-9.7), follow-up time (15+/-9.0 months vs. 18+/-10), gender (female:male 8:7 vs. 15:19), aortic valve gradient on Doppler (70.0+/-20 mmHg vs. 71+/-20) and left ventricular mass (360+/-118 g vs. 320+/-80) between the two groups (all P=NS). Left ventricular shortening fraction (22+/-9.0% vs. 28+/-8.5, P<0.05), ejection fraction (51+/-15% vs. 62+/-12, P<0.01) and circumferential fibre shortening (0.8+/-0.3 circ/s vs. 1.0+/-0.3, P<0.0s) were all significantly reduced in patients with right precordial Q waves compared to those without. During a mean follow-up of 1.5 years, 9 out of 15 (60%) patients with right precordial Q waves died compared with only 5 out of 34 (15%) patients with a normal QRS pattern died (P<0.01). In summary, a right precordial QS ECG pattern is present in nearly 1/3 patients with aortic stenosis and is associated with impaired left ventricular systolic function and adverse prognosis.