Efficacy of Apneic Oxygenation During Pediatric Endotracheal Intubation.

OBJECTIVE: Because of the abundance of complications associated with peri-intubation hypoxia, maintaining adequate oxygen saturation during endotracheal intubation (ETI) is of great concern. In addition to standard preoxygenation techniques, apneic oxygenation (AO), the continuous flow of passive oxygenation, is a potential tool that can be used to eliminate hypoxia during ETI. Although scarcely studied in the pediatric population, AO has proven effective in reducing the incidence of hypoxia in adult patients with minimal side effects. The objective of this study is to evaluate the use of apneic oxygenation in pediatric patients and to determine its efficacy in preventing or delaying oxygen desaturation during the apneic period of ETI. METHODS: This literature review examines 4 studies that evaluate the practice of AO in pediatric patients. A total of 712 patients across 3 randomized control trials and 1 observational study were assigned to either a control group that did not receive any form of AO, a group that did not receive 100% fraction of inspired oxygen (FiO2), or an intervention group where various methods of AO were delivered. RESULTS: Each AO method that provided 100% FiO2 saw a significantly longer time until initial desaturation when compared with those that did not receive any form of AO or those not receiving 100% FiO2. CONCLUSIONS: The findings in this study confirm that the practice of AO is not only efficacious in increasing the time until initial desaturation but also reduces the overall incidence of hypoxia during laryngoscopy in children.

From volume to value? Can a value-based approach help deliver the ambitious aims of the NHS cardiovascular disease outcomes strategy?

The last year has seen the publication of two papers which will radically shape the future organisation of healthcare in general, and cardiovascular disease in particular: Cardiovascular Outcomes Strategy (Department of Health) and The Strategy That Will Fix Healthcare (Harvard Business Review). Both publications set out a health delivery mechanism based around improvement of outcomes for groups of patients with similar needs. Instead of organising care around disease categories, it is proposed that the cardiovascular diseases are treated as a single family of diseases. We are reaching the limits of what an activity-based system organised around existing provider structures can sustainably deliver. Unless we find delivery systems which reduce costs while at the same time improving outcomes that are meaningful to patients, then we will be faced with a future of healthcare rationing. The increasing burden of chronic disease and ongoing quality concerns in delivery systems has created a 'burning platform', which must be addressed if we are to maintain a system which offers high-quality care free at the point of delivery. This paper explores what an outcomes and value-based system could look like when applied to cardiovascular disease. It explores what it means for providers and patients if we start to think about outcomes by patients with similar needs, rather than by intervention, or by clinical specialty. As a specific example, the paper explores the features of an Integrated Circulation Service, what the challenges and implications might be, and whether there is any evidence that this would deliver improved outcomes, at a lower cost to the system.

Atrial septal aneurysm and patent foramen ovale are less prevalent in the Indo-Asian than in the Caucasian or Afro-Caribbean population.

UNLABELLED: Atrial septal aneurysm (ASA) and patent foramen ovale (PFO) are not uncommon during routine echocardiographic scanning and were reported to be associated with stroke, transient ischemic attacks, and migrainous headache. To assess the prevalence of ASA and PFO according to ethnicity, we retrospectively studied 887 consecutive referrals to a General Cardiology and Hypertension clinics. All participants underwent trans-thoracic echocardiography (TTE). In some patients, the TTE was repeated using bubble contrast. RESULTS: Atrial septal aneurysm was detected in 70 participants (7.9%) and PFO in 18 (2%). Atrial septal aneurysm, PFO, or their combination was detected in 12% of the Caucasian patients, 15% of the Afro-Caribbean, and 3.7% of the Indo-Asian patients. CONCLUSIONS: There was a lower prevalence of ASA and PFO and their combination in Indo-Asians and a higher rate in Afro-Caribbeans than in Caucasians. The higher prevalence in the Afro-Caribbean participants may contribute to the high incidence of stroke in black participants.

Right ventricular stunning in inferior myocardial infarction.

AIM: To assess right ventricular (RV) function in patients with inferior myocardial infarction (IMI) and to observe changes following thrombolysis. BACKGROUND: RV dysfunction occurs in 30% of patients with IMI. The extent of such involvement and its potential, recovery has not been determined. METHODS: We studied 30 patients with acute IMI (age 56+/-12 years), on admission, day 7 and day 30 post thrombolysis. No patient had clinical signs of RV failure. RV segmental function was assessed from free wall long axis and global function from filling and ejection velocities. Values were compared with 15 age-matched controls. RESULTS: On admission, RV long axis amplitude, systolic and diastolic velocities were depressed (2.09+/-0.39 vs 2.6+/-0.3 cm, 8.18+/-1.8 vs 10.0+/-2.0 cm/s and 6.9+/-2.7 vs 10.0+/-2.5 cm/s, p<0.01 for all) and global function impaired; reduced Z ratio (0.85+/-0.07 vs 0.9+/-0.04, p<0.01), raised Tei index (0.49+/-0.26 vs 0.3+/-0.1, p<0.001) and prolonged t-IVT (8.16+/-3.9 vs 4.8+/-2 s/m, p<0.01) compared to controls. After thrombolysis, RV long axis amplitude (2.28+/-0.3 cm, p<0.05), systolic velocity (10.0+/-2.7 cm/s, p<0.01), early diastolic velocity (8.3+/-2.16, p<0.05), Z ratio (0.9+/-0.05, p<0.01), Tei index (0.34+/-0.17, p<0.01) and t-IVT (6.2+/-2.7 s/m, p<0.05) all normalised at day 30. Only 4 (13%) patients remained with RV long axis amplitude and one with t-IVT and Tei index values outside the normal 95% CI at day 30. RV inflow diameter and tricuspid regurgitation did not change. CONCLUSION: In IMI, RV segmental and global functions are acutely impaired, and recover in 87% of patients following thrombolysis. In the absence of clear evidence for RV infarction the disturbances in the remaining 13% may represent stunned myocardium that may demonstrate delayed recovery.

Ventricular endocrine and mechanical function following thrombolysis for acute myocardial infarction.

OBJECTIVE: The objective of this study was to assess natriuretic peptide release following acute myocardial infarction, and its relationship with ventricular function. METHODS: A total of 44 patients with acute myocardial infarction were studied; 13 anterior, age (57+/-12 years) and 31 inferior, age (58+/-12 years). Peptide levels and left ventricular function by echocardiography were assessed at admission and on days 7 and 30 after thrombolysis. Healthy volunteers (n=21) served as controls. RESULTS: Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) levels rose from admission to day 7 (p=0.002). While ANP remained elevated at day 30 in both groups, BNP levels fell in patients with anterior myocardial infarction (p=0.03). Left ventricular fractional shortening was reduced at admission in the two groups (p=0.01) but returned towards normal in 7 days (p=0.001) in inferior myocardial infarction and in 30 days in anterior myocardial infarction (p=0.02). Left ventricular long axis amplitude was universally reduced at admission (p=0.01) and remained abnormal at day 30 (p=0.01) in both groups. At day 7, BNP and ANP levels inversely correlated with long axis amplitude of lateral wall in anterior myocardial infarction; (r=-0.7, p=0.01). BNP correlated inversely with fractional shortening in anterior myocardial infarction (r=-0.7, p=0.01) at day 30. CONCLUSION: The elevated peptide levels at 7 days post-myocardial infarction correlate with reduced mechanical activity of the adjacent noninfarcted segment. Natriuretic peptides release seem to be related to failure of compensatory hyperdynamic activity of the noninfarcted area rather than directly from the injured myocardial segments.

Is glycated haemoglobin a sensitive index to identify left ventricular dysfunction two months after acute myocardial infarction in normotensive subjects?

BACKGROUND: Glycated haemoglobin concentration (HbA1c) is a marker of glucose metabolism. Glucose intolerance is associated with a high incidence of left ventricular (LV) dysfunction after acute myocardial infarction (AMI). This study was carried out in order to relate HbA1c to LV function two months following AMI in 171 normotensive patients who were not previously known to have had diabetes mellitus. METHODS: Oral glucose tolerance test (GTT) and HbA1c. Echo and Doppler-cardiography were used to measure the E/A (peak velocity of the early filling/atrial contraction waves) at rest and at peak isometric exercise (IME), deceleration time (DT) of E wave, LV ejection fraction (LVEF), LV mass index and diastolic LV function. RESULTS: GTT was diabetic in 20, impaired in 35 and normal in 116 subjects. HbA1c was >6.0% (cut off level for high risk subjects) in 76 patients (67%) with impaired relaxation (E/A<1) during IME and in 30 patients (27%) with restrictive LV filling (identified by E/A=1-2, DT<140 ms). The sensitivity and specificity of HbA1c to predict underlying impaired LV relaxation were 68% and 37%, respectively, and to predict restrictive LV filling were 27% and 98%, respectively. Whereas in univariate analysis, DT.3 was linearly related to HbA1c only (p=0.0002), multiple regression analysis showed that HbA1c was related to LVEF, DT and E/A but not to LVH, LVMI, smoking habit, age, gender and creatinine kinase level during admission for AMI. CONCLUSION: At 2 months after admission for AMI, HbA1c is related to systolic and diastolic LV function but not to LVMI or LVH. HbA1c is a sensitive predictor of impaired relaxation but highly specific to rule out underlying non-restrictive LV filling.

Combination of site of infarct, unrecognized glucose intolerance, and reinfarction after acute myocardial infarction in normotensive subjects is determinant of the development of subsequent systemic hypertension: a pilot study.

BACKGROUND: The natural history of hypertension in healthy normotensive subjects has been described in the Framingham population. We aim to study the rate of progression to hypertension in normotensive subjects after acute myocardial infarction (AMI). METHODS: One hundred seventy-three consecutive normotensive subjects admitted to the Coronary Care Unit with AMI were studied retrospectively with prospective follow-up 4 years after AMI. All the patients who were not known to be diabetic on admission (n = 150) underwent glucose tolerance test (GTT) at 2 months after AMI. RESULTS: Among the 15 patients (8.7%) who developed hypertension, GTT was abnormal in 75% (diabetes = 3, impaired glucose tolerance = 9). There were significantly more Indo-Asians and fewer whites in the hypertensive than in the normotesive patients but they were similar in age and gender, creatinine kinase level, and rate of thrombolysis during admission for AMI. Multiple regression analysis showed that progression to hypertension was a function of the presence of anterior AMI on admission (P = .0297), abnormal GTT (P = .0156), and subsequent MI on follow-up (P = .0122), but was independent of age, gender, smoking habit, body weight, previous MI, thrombolysis, creatinine kinase level, subsequent development of heart failure, and intake of beta-adrenergic blockade or angiotensin-converting enzyme (ACE) inhibitor. Of the hypertensive patients, 47% (n = 7) died compared to 8% (n = 13) of the normotensive subjects (P < .0001). CONCLUSIONS: Progression to hypertension in normotensive subjects after AMI is determined by a combination of the site of the infarct, GTT 2 months after AMI, and subsequent development of a second MI. Systemic hypertension after AMI is associated with a high mortality.

Left ventricular hypertrophy and preclinical impaired glucose tolerance and diabetes mellitus contribute to abnormal left ventricular diastolic function in hypertensive patients.

BACKGROUND: Impaired left ventricular diastolic function is not uncommon in patients with either diabetes mellitus or hypertension. This study was carried out to assess the contribution of left ventricular hypertrophy, high blood pressure, preclinical impaired glucose tolerance and diabetes mellitus to left ventricular diastolic function in patients attending a hypertension clinic. METHODS: Echocardiography, 24-h ambulatory blood pressure monitoring and oral glucose tolerance tests were carried out in 152 consecutive hypertensive patients who had no evidence of ischaemic heart disease and were not known to be diabetic. From echocardiography, E/A (peak velocity of early/atrial filling waves of the transmitral flow) at rest and at peak standardized isometric exercise using handgrip, left ventricular mass index and deceleration time of the E wave were derived. RESULTS: Patients with impaired glucose tolerance and diabetes mellitus had lower E/A than the euglycaemic subjects both at rest (P=0.0073) and during isometric exercise (P<0.0001). E/A significantly reduced during isometric exercise in patients with impaired glucose tolerance and diabetes but not in euglycaemic patients. Deceleration time was shortened with a worsening degree of glucose intolerance in all the patients (P=0.0005), in those with left ventricular hypertrophy (P=0.0006) and in those without left ventricular hypertrophy (P=0.033). When adjusted for age, gender, race, body mass index, smoking history, ambulatory blood pressure findings, cholesterol and triglyceride levels and antihypertensive medications taken, E/A at isometric exercise was related to results of glucose tolerance tests and was inversely proportional to left ventricular mass index (P<0.0001). No significant differences were found whether patients were taking antihypertensive medications or not. CONCLUSION: In hypertensive patients, left ventricular diastolic function is determined by left ventricular mass index and the status of preclinical glucose intolerance, independent of age, gender, race, body mass index, blood pressure level, nocturnal drop in blood pressure or lipid level. These findings were not prejudiced by antihypertensive medications.

The glucose tolerance test, but not HbA(1c), remains the gold standard in identifying unrecognized diabetes mellitus and impaired glucose tolerance in hypertensive subjects.

The objective of this study was to compare the value of the oral glucose tolerance test (GTT), glycated hemoglobin concentration (HbA(1c)), and fasting plasma glucose (FPG) for identifying unrecognized diabetes mellitus (DM) and impaired glucose tolerance (IGT) in hypertensive subjects. One hundred forty-four consecutive subjects who were not known to have DM and who were attending the Hypertension Clinic underwent 24-hour ambulatory blood pressure (BP) monitoring. A GTT and an HbA(1c) measurement were also carried out. Abnormal results from GTT were found in 94 patients (65%). Results from FPG were not different between those with DM and IGT but were significantly higher than in the euglycemic subjects. The FPG was between 110-125 mg/dL (6.1-6.9 mmol/L) in 31% (n = 20) of patients with IGT and in 53% (n = 16) of those with DM. With use of the previously published criteria to diagnose DM of FPG > or = 103 mg/dL (5.7 mmol/L) and HbA(1c) > or = 5.9%, 33% of our diabetic subjects and 75% of those with IGT would have been misclassified as euglycemic. The previously reported cut-off point for HbA(1c) of >6.1% to diagnose DM was present in 77% of our patients with DM and in 14% (n = 9) of the patients with IGT. Multiple regression analysis showed that an abnormal result from GTT was independent of the level of clinical or ambulatory BP, nocturnal BP dip, cholesterol level, smoking history, race, or class of antihypertensive medication taken. FPG levels or HbA(1c), or their combination, are not accurate enough to identify DM or IGT in patients attending a hospital Hypertension Clinic. A GTT may be required in these patients to reliably identify those with DM or IGT.

Left ventricular diastolic function in normotensive subjects 2 months after acute myocardial infarction is related to glucose intolerance.

BACKGROUND: Both glucose intolerance and myocardial infarction are independently associated with impaired left ventricular (LV) function. This study was carried out to relate LV diastolic function in normotensive subjects 2 months after acute myocardial infarction (AMI) to glucose tolerance status. METHODS: Left ventricular ejection fraction (LVEF), LV mass index, peak velocity of the early phase/atrial contraction wave, deceleration time of E wave, and isovolumic relaxation time were measured during echocardiograph/Doppler cardiography in 200 normotensive patients 2 months after AMI. Twenty-nine patients were known to be diabetic on admission with AMI. Glucose tolerance test was carried out in the 171 patients who are not known to be diabetic. RESULTS: Independent of LVEF, restrictive LV filling (peak velocity of the early phase/atrial contraction wave > 1 but < 2 associated with deceleration time of E wave < or = 140 milliseconds) was found in 72% of the known-diabetic patients, 70% of the 20 preclinical diabetic patients, 23% of the 35 patients with impaired glucose tolerance, 13% of the 15 patients with stress hyperglycemia, and 7% of the euglycemic patients (P < .01). In the rest of these patients, LV filling was nonrestrictive. No significant difference was observed in LVEF and LV mass index between patient groups. CONCLUSION: Independent of LVEF, the pattern of abnormal LV filling in normotensive subjects 2 months after AMI is a function of the severity of glucose intolerance, restrictive in the majority of the diabetic patients and nonrestrictive in the majority of the euglycemic patients, impaired glucose tolerance, and stress hyperglycemia. After AMI, abnormal LV filling occurs even in the absence of detectable systolic dysfunction or left ventricular hypertrophy.

Impaired left ventricular diastolic function during isometric exercise in asymptomatic patients with hyperlipidaemia.

BACKGROUND: Left ventricular (LV) diastolic dysfunction is an early sign, and may be more sensitive indicator, of ischaemic heart disease (IHD) than systolic dysfunction. METHODS: LV diastolic function was assessed during isometric exercise (IME) in 37 consecutive normotensive hyperlipidaemics (LIP), without cardiac history or symptoms. Each patient underwent a stress ECG test and 2-D echo and Doppler cardiography. During the latter, transmitral flow at rest and at peak standardised IME using handgrip was studied. From the tracings, the E/A (peak velocity of the early/atrial components), the contribution of atrial systole to LV filling (ACF), the deceleration time (DT) of the E wave and the isovolumic relaxation time (IVRT) were calculated. Results were compared to 37 age-matched normal healthy volunteers (NOR). RESULTS: Resting E/A was not different between NOR and the LIP. A significant reduction in E/A with IME was observed in LIP but not in NOR. Impaired LV filling (shown by E/A<1) was demonstrated in five patients (13%) at rest and in 20 patients (54%) at peak IME. All NOR had E/A>1 suggesting normal LV filling. Fifteen of the 30 patients with negative stress ECG test demonstrated LV diastolic dysfunction. ACF was higher in LIP than NOR and increased significantly (P<0.005) by 23% during IME. DT and IVRT in LIP were not different from NOR. In neither NOR nor LIP, were the LV diastolic functional parameters related to gender, smoking habit or levels of total cholesterol, LDL- or HDL-cholesterol or triglycerides. CONCLUSION: The prevalence of LV diastolic dysfunction in asymptomatic patients with hyperlipidaemia despite a negative stress ECG test may be evidence of early underlying pre-clinical myocardial ischaemia.

Prevalence of unrecognized abnormal glucose tolerance in patients attending a hospital hypertension clinic.

BACKGROUND: Diabetes mellitus (DM) and impaired glucose tolerance (IGT) are not uncommonly associated with hypertension. Fasting blood glucose level is still recognized as an indicator of DM. METHODS: We studied 99 consecutive patients who were not known to be diabetic patients and with no cardiac history, who were attending our Hypertension Clinic for investigation and management of uncontrolled blood pressure (BP). Oral glucose tolerance test (GTT) was carried out and area under the curve for the GTT (AUC-glucose) was calculated. All patients underwent 24-h ambulatory BP monitoring. RESULTS: The GTT was abnormal in 58 patients (58%), indicating IGT in 18, impaired fasting glucose in 16, and DM in 24. The fasting and 120-min glucose level and AUC-glucose in patients with DM on GTT was higher (P <.0001) than in those with IGT/IFG and in the latter was higher than those with normal GTT. Multiple regression analysis showed that abnormal GTT was independent of the following: level of clinic or ambulatory BP; presence or absence of nocturnal BP dip; cholesterol, sodium, and potassium levels; smoking history; alcohol intake; prior treatment for hypertension; and ethnicity. These results were also independent of antihypertensive medications taken. No significant difference was found in glucose level during GTT, AUC-glucose, or age among the groups of patients receiving diuretics only, those receiving diuretics and beta-blockers, and those not receiving any of these agents. CONCLUSIONS: The prevalence of glucose abnormalities in hypertensive patients attending a hospital hypertension clinic is sufficiently high to warrant screening for DM and IGT, and fasting glucose levels are not accurate enough for this purpose. All patients attending such a clinic should undergo a GTT.

The degree of albuminuria is related to left ventricular hypertrophy in hypertensive diabetics and is associated with abnormal left ventricular filling: a pilot study.

The association of albuminuria and left ventricular (LV) hypertrophy (LVH) in diabetics aggravates the prognosis. The authors studied the relation between LVH and the degree of albuminuria in diabetics and investigated the relationship of albuminuria to LV filling. A comparison was made between 30 hypertensive diabetics, 10 of whom had microalbuminuria (MIC) and 20 had macroalbuminuria (MAC), and 18 diabetics who were normotensive and normalbuminuric (NOR). LV mass index (LVMI) and LV ejection fraction (LVEF) were measured during echocardiography. LV filling pattern at rest and at peak standardized isometric exercise (IME) using handgrip was assessed by measuring E/A (peak velocity of the early/atrial filling waves) of the transmitral flow during Doppler and echocardiography. Each patient underwent a stress ECG test. LVMI was higher in MAC (132.3 +/- 55.4) than in MIC (115.6 +/- 32.5) or NOR (90.0 +/- 31.8) (p<0.01). There were more patients in MAC with LVH (n = 13) and abnormal filling (n = 9 at rest and 16 with IME) than in MIC (LVH = 5, abnormal filling = 1 at rest and 10 during IME) or NOR (LVH = 3, abnormal filling = 1 at rest and 9 during IME) (p < 0.02). LVMI was not related to LVEF. Although blood pressure was not different between MAC and MIC groups, it was significantly higher than in the NOR group. This study suggests that a high degree of albuminuria in hypertensive diabetics is associated with greater value for LVMI and an increased incidence of LVH independent of blood pressure level or systolic LV function. LVH is associated with abnormal LV filling. The degree of albuminuria may predict LVMI and LVH, which are associated with abnormal LV filling. This association of abnormal LV filling with albuminuria in hypertensive diabetic patients may account for their high risk of cardiovascular events.

Age-associated changes in left ventricular diastolic function are related to increasing left ventricular mass.

Isometric exercise (IME) produces significant hemodynamic changes in the cardiovascular system. We have used IME to study the effect of age on diastolic left ventricular (LV) function in 100 normal volunteers. The E/A ratio (peak velocity of early/atrial filling phases), deceleration time (DT), and isovolumic relaxation time (IVRT) of the transmitral flow were assessed during echocardiography with pulsed-Doppler ultrasound at rest and at peak IME using handgrip. LV mass index (LVMI) and LV ejection fraction (LVEF) were also calculated. Both E/A and IVRT reduced significantly with increasing age. The LVEF decreased (P <.0001), whereas LVMI increased (P <.05) with advancing age. The LVEF was inversely related to LVMI (P <.05). An inverse relationship was noted between E/A and LVMI (P <.01) during IME. The contribution of the atrial contraction to the total diastolic flow increased significantly with advancing age (P <.02) and increased from 0.29 +/- 0.04 at rest to 0.34 +/- 0.08 during IME (P <.0001). It is concluded that with progressing age, the left ventricle becomes stiffer resulting in a reduction in early filling and a compensatory increase in flow due to atrial contraction. A progressive increase in LVMI, which accompanies aging may contribute to stiffening of the left ventricle and deterioration in diastolic function of the left ventricle. This is exaggerated by IME.

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.