Diagnostic Concordance and Clinical Outcomes in Patients Undergoing Fractional Flow Reserve and Stress Echocardiography for the Assessment of Coronary Stenosis of Intermediate Severity.

BACKGROUND: The ischemic consequences of coronary artery stenosis can be assessed by invasive fractional flow reserve (FFR) or by noninvasive imaging. We sought to determine (1) the concordance between wall thickening assessment during clinically indicated stress echocardiography (SE) and FFR measurements and (2) the factors associated with hard events in these patients. METHODS: Two hundred twenty-three consecutive patients who underwent SE and invasive FFR measurements in close succession were analyzed retrospectively for diagnostic concordance and clinical outcomes. RESULTS: At the vessel level, the sensitivity, specificity, positive predictive value, and negative predictive value of SE for identifying significant disease as assessed by FFR was 68%, 75%, 43%, and 89%, respectively. The greatest discordance was seen in patients with wall thickening abnormalities (WTAs) and negative FFR. During a follow-up of 3.6 ± 2.2 years, there were 23 cardiovascular (CV) events (death and nonfatal myocardial infarction). The number of wall segments with inducible WTAs emerged as the strongest factor associated with CV events (hazard ratio, 1.18 [1.05-1.34]; P = .008). FFR was not associated with outcome. There was a significant increase in event rate in patients with WTA/negative FFR versus no WTA/negative FFR (P = .01), but no significant difference versus WTA/positive FFR (P = .85). CONCLUSIONS: In a patient population with significant CV risk factors, a normal SE had a high negative predictive value for excluding abnormal FFR. WTAs were associated with outcomes regardless of FFR value, suggesting that this is a superior marker of ischemia to FFR.

The clinical impact of contemporary stress echocardiography in morbid obesity for the assessment of coronary artery disease.

OBJECTIVE: Non-invasive cardiac imaging may suffer from poor image quality in morbidly obese individuals. This study aimed to determine the clinical value of contemporary stress echocardiography (SE) in morbidly obese patients referred for assessment of suspected coronary artery disease (CAD). METHODS: This prospective, multicentre observational study was conducted in two district hospitals and one tertiary centre in London, UK. Individuals with body mass index ≥35 kg/m(2) referred for SE were evaluated. The percentage of patients with obstructive CAD on coronary angiography, following abnormal SE, was assessed. Patient outcomes were determined with follow-up for the composite end-point of all-cause mortality, myocardial infarction and late revascularisation. RESULTS: Over a 13-month period, 209 morbidly obese patients underwent SE, and contrast agent was used in 96% of patients. A diagnostic result was obtained in 200/209 (96%) patients. Of 32 (15%) patients with inducible ischaemia, 25 underwent angiography, 22 (88%) had corresponding significant CAD and, of these, 16 (77%) underwent revascularisation. Conversely, only 2/157 patients (1.3%) with normal SE underwent angiography, and none underwent revascularisation. Over a mean follow-up period of 17.8±5.4 months, there were nine events. The annualised cardiac event rate after a normal SE was 0.95%. Events were more frequent in patients with inducible ischaemia versus those without ischaemia (5/32 (15.6%) vs 4/153 (2.6%); p=0.002). Ejection fraction <50% (HR 9.5; 95% CI 2.4 to 38.0; p=0.002) and inducible ischaemia (HR 9.4; 95% CI 2.5 to 35.8; p=0.001) were predictors of outcome on univariable Cox regression analysis. CONCLUSIONS: Contemporary SE has excellent feasibility and positive predictive value and resulted in appropriate risk stratification of symptomatic patients with significant obesity. A normal SE portends an excellent outcome over the short-intermediate term in this high-risk patient population.

Incremental diagnostic and prognostic value of contemporary stress echocardiography in a chest pain unit: mortality and morbidity outcomes from a real-world setting.

BACKGROUND: Clinical assessment often cannot reliably or rapidly risk stratify patients hospitalized with suspected acute coronary syndrome. The real-world clinical value of stress echocardiography (SE) in these patients is unknown. Thus, we undertook this study to assess the feasibility, safety, ability for early triaging, and prediction of hard events of SE incorporated into a chest pain unit for patients admitted with acute chest pain, nondiagnostic ECG, and negative 12-hour troponin. METHODS AND RESULTS: Accordingly, 839 consecutive patients who underwent clinical, ECG, and SE assessments within 24 hours of admission were assessed for feasibility, safety, impact on triaging and discharge, and 30-day readmission rate and were followed up for hard events (all-cause mortality and acute myocardial infarction). Of the 839 patients, 811 (96.7%) had diagnostic SE results. Median time to SE and median length of stay for normal SE patients (77%) were both 1 day. The 30-day readmission rate was 0.5%. During long-term follow-up of 27±11 months, 39 hard events (30 deaths and 9 acute myocardial infarctions) occurred. Kaplan-Meier estimates of hard events were 0.5% versus 6.6% in the normal versus abnormal SE groups, respectively, in the first year of follow-up (15 events in the first year). Among all prognostic variables, only abnormal SE (hazard ratio, 4.08; 95% confidence interval, 2.15-7.72; P<0.001) and advancing age (hazard ratio, 1.78; 95% confidence interval, 1.39-2.37; P<0.001) predicted hard events in multivariable regression analysis. CONCLUSIONS: SE incorporated into a chest pain unit has excellent feasibility and provides rapid assessment and discharge with accurate risk stratification of patients with suspected acute coronary syndrome but nondiagnostic ECG and negative 12-hour troponin.

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.

The effect of the Q wave infarct on left ventricular electromechanical function.

OBJECTIVE: To assess the nature of left ventricular (LV) electrical and mechanical dysfunction in Q compared to non-Q anterior myocardial infarction (MI). SUBJECTS: We used ECG and echocardiography to study 54 unselected patients, age 57+/-15 years, 32 male, with old (>6 months after) anterior MI (39 Q and 15 non-Q), confirmed by enzyme rise and regional wall motion abnormality, and compared them with 21 normals of similar age. METHODS: Analysis of resting LV minor and long axis function and 12-lead surface electrocardiogram. RESULTS: Only 10% of normals did not have a normal septal Q wave compared with 46% of non-Q wave MI and 84% Q wave MI (P<0.001). All patients with Q wave MI had a scarred anteroseptal wall but none of the non-Q wave MI. LV minor axis dimensions were increased only with Q wave MI: 6.0 +/- 0.9 vs. 4.9 +/- 0.5 cm at end-diastole and 4.5 +/- 1.1 vs. 3.3 +/- 0.5 cm at end-systole and fractional shortening was reduced 27 +/- 8 vs. 33 +/- 3% (P<0.001 for all). Total left ventricular long axis amplitude of motion was reduced at the left, septal and posterior sites only in Q wave MI but was not different from controls in non-Q wave MI. The onset of long axis shortening was delayed by 20 ms at the left and septal sites in non-Q wave MI and by an additional 20 ms at the three sites in Q wave MI. Peak long axis shortening rate was reduced in the two patient groups, with the same distribution as post-ejection shortening (greater than 1 mm), which occurred in 21% of patients with non-Q wave MI and 76% of patients with Q wave MI (P<0.001). In diastole, the onset of long axis lengthening was delayed by 20 ms at the left and septal sites in non-Q wave MI and at the three sites in Q wave MI (P<0.001). Peak long axis lengthening rate was reduced with a similar distribution in the two patient groups. CONCLUSION: Patients with Q wave MI have an increased LV dimension and reduced FS, whereas patients with non-Q wave MI appear to have morphologically normal LV minor axis dimensions and fractional shortening apart from the anterior wall hypokinesis. In the latter, however, long axis function shows significant systolic and diastolic disturbances affecting the anteroseptal and lateral walls. The absence of conduction disturbances in non-Q wave MI suggests intrinsic myocardial dysfunction that may be reversible.

The effect of the localization of Q wave myocardial infarction on ventricular electromechanics.

BACKGROUND: The exact location of a Q wave myocardial infarction has an important effect on overall left ventricular function. OBJECTIVES: To assess the effect of localization of Q wave infarction on left ventricular minor and long axis function, with particular reference to electromechanical disturbances. METHODS: We studied 72 patients with Q wave myocardial infarction; 35 anterior, age 61+/-15 years and 37 inferior, age 62+/-12 years. ECG intervals were automatically measured by Hewlett-Packard Pagewriter and LV dimension and filling velocities studied by transthoracic echocardiography and simultaneous phonocardiogram. Findings were compared with 21 controls of similar age. RESULTS: Heart rate and all ECG intervals were similar in the two patient groups and controls. QRS axis was more to the left in patients with inferior MI. Normal septal q wave was absent in lead V5 and V6 in 33/35 (94%) patients with anterior MI and in only 3/37 (8%) with inferior MI, p<0.001. LV minor axis dimensions were enlarged vs. normal (p<0.001) in the two patient groups and to a greater extent in anterior MI compared with inferior MI, p<0.05. Isovolumic relaxation time was prolonged only in-patients with an inferior MI, p<0.01. Long axis amplitude was globally reduced (p<0.001) in the two patient groups as were shortening and lengthening velocities (p<0.001). The onset of septal long axis shortening with respect to the q wave was delayed by 30 and 40 ms in inferior MI and anterior MI and that of lengthening with respect to A2 by 20 and 30 ms, respectively, compared to normal (p<0.001 for both). Post ejection shortening was localized to the septal long axis in 32/35 patients with anterior MI but was generalized involving all three LV long axes in inferior MI, p<0.001. Transmitral Doppler flow velocities and the frequency of mild mitral regurgitation were similar in the two groups. CONCLUSION: These results confirm a close association between anterior Q wave infarction, septal incoordination and absent septal q waves. The global incoordinate long axis behaviour in inferior Q wave MI may be due to significant papillary muscle dysfunction, and results in significant shape change in early diastole. This disturbance in electromechanical behaviour might play an important role in the differing outcomes between the two different sites of myocardial infarction.

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.