Evaluation of right atrial volumes and functions by real-time three-dimensional echocardiography in patients after acute inferior myocardial infarction.

BACKGROUND: Right ventricle (RV) involvement causes acute systolic and diastolic functional alterations in the RV in patients after inferior myocardial infarction (IMI), which may result in an increase in left ventricle (LV) end-diastolic and right atrial (RA) pressure. In our study, we sought to evaluate RA volumes and mechanical functions using real-time three-dimensional echocardiography (RT3DE) in IMI patients with or without RV involvement. METHODS: Ninety-six consecutive patients with IMI (mean age: 59.7 ± 10.2 years, 60 female) were included. RV myocardial involvement (RVMI) was defined as the presence of a culprit lesion at the proximal portion of the first RV marginal branch in coronary angiography. The study population was divided into two groups: IMI (58.3%) and IMI + RVMI (41.7%). Patients were evaluated using conventional two-dimensional echocardiography (2DE) and RT3DE. RESULTS: In RT3DE measurements, IMI + RVMI patients had significantly higher RA phasic volumes and worse conduit mechanical function. A receiver operating characteristic (ROC) curve analysis revealed that an RT3DE RA maximum volume (Vmax) index > 27.9 mL/m2 was an independent predictor of RV involvement in patients after acute IMI, with a sensitivity of 80.0% and a specificity of 89.3%. CONCLUSIONS: Right ventricle involvement may cause an increase in RA phasic volumes and deterioration of conduit function in patients with acute IMI.

Correlation of ST changes in leads V4-V6 to area of ischemia by CMR in inferior STEMI.

OBJECTIVE: We aim to determine the correlation between ST-segment changes in leads V4-V6 and the extent of myocardial injury by cardiac magnetic resonance (CMR) in patients with inferior ST elevation (STE) myocardial infarction (iSTEMI). DESIGN: Admission electrocardiogram and CMR data from the MITOCARE trial were used. Differences in mean myocardium at risk, infarct size, ejection fraction and myocardial segment involvement by CMR were compared in patients with first iSTEMI with STE, ST depression (STD) or no ST changes (NST) in V4-V6. Myocardial segment involvement was further evaluated by comparing proportion of patients in each group with ≥25% and ≥50% segment involvement. RESULTS: Fifty-four patients were included. Patients with STE (n = 22) and STD (n = 16) in V4-V6 had significantly lower ejection fraction compared to NST (n = 16) (48% vs 48% vs 54%, p = .02). STE showed more apical, apical lateral and mid-inferolateral involvement but less basal inferior involvement than NST. STD exhibited greater basal inferoseptal involvement compared to STE. There were more patients with STE that had ≥25% and ≥50% apical lateral involvement compared with STD and NST groups. Patients with STD were more likely to have ≥25% and ≥50% basal inferoseptal involvement compared with STE and NST groups. CONCLUSION: Our study suggests that in iSTEMI, ST changes in the precordial leads V4-V6 correlates with greater myocardial injury and distribution of myocardium at risk.

Attenuation correction in myocardial perfusion imaging affects the assessment of infarct size in women with previous inferior infarct.

BACKGROUND: Myocardial perfusion imaging is a well-established diagnostic tool in patients with known or suspected coronary artery disease. Numerous clinical trials have shown that attenuation correction (AC) in single photon emission computed tomography (SPECT) improves the diagnostic accuracy of myocardial perfusion imaging over non-AC SPECT, differentiating between scar and attenuation artifacts. We have previously shown that attenuation artifacts produce an overestimation of the size of inferior infarcts in the male population. It is assumed that women are less affected by inferior attenuation artifacts than men. PURPOSE: The aim of this study is to evaluate the role of AC in the assessment of infarct size in female patients with a history of myocardial inferior infarct. PATIENTS AND METHODS: We studied a population of 66 consecutive women, with a history of previous inferior myocardial infarct, by SPECT/computed tomography (CT) with 370+370 MBq of technetium-99m labeled compounds by a 2-day stress-rest protocol. Both AC and uncorrected gated-SPECT/CT studies were reconstructed after scatter and motion correction by ordered-subset expectation maximization iterative reconstruction and resolution recovery. The coregistration of the transmission and emission scans was verified for all patients; any misalignment was realigned manually. Uncorrected and corrected SPECT images were analyzed by software QPS/QGS package using a 17-segment model. For each segment, perfusion and wall motion were quantified using a five-point score according to the American Society of Nuclear Cardiology guidelines. Summed stress, summed rest score (SRS), and summed difference score of the inferior left ventricle wall (inferior, inferoseptal, inferolateral, and apical inferior segments) were calculated. A linear correlation was used to assess the relationship between perfusion and the regional wall motion score as determined by uncorrected gated-SPECT. RESULTS: The results of quantitative analysis of non-AC and CT-AC SPECT images, respectively, were as follows: summed stress score: 9.47±5.01 and 6.58±4.77% (P<0.001); SRS was 6.05±5.02 and 4.14±4.12% (P<0.001); the summed difference score was 2.92±2.74 and 2.52±2.63% (P=NS), respectively. The correlation between corrected and uncorrected SRS and the regional summed wall motion score of the same segment was R=0.31 versus R=0.34. CONCLUSION: In the female population, like in men, attenuation artifacts affect the calculation of the infarct size of the inferior wall, with overestimation of the infarct size in uncorrected images. The AC regional perfusion score (SRS) better correlates with the regional wall motion score of the inferior wall in women with previous inferior infarct.

Cardiac αVß3 integrin expression following acute myocardial infarction in humans.

OBJECTIVE: Maladaptive repair contributes towards the development of heart failure following myocardial infarction (MI). The αvß3 integrin receptor is a key mediator and determinant of cardiac repair. We aimed to establish whether αvß3 integrin expression determines myocardial recovery following MI. METHODS: 18F-Fluciclatide (a novel αvß3-selective radiotracer) positron emission tomography (PET) and CT imaging and gadolinium-enhanced MRI (CMR) were performed in 21 patients 2 weeks after ST-segment elevation MI (anterior, n=16; lateral, n=4; inferior, n=1). CMR was repeated 9 months after MI. 7 stable patients with chronic total occlusion (CTO) of a major coronary vessel and nine healthy volunteers underwent a single PET/CT and CMR. RESULTS: 18F-Fluciclatide uptake was increased at sites of acute infarction compared with remote myocardium (tissue-to-background ratio (TBRmean) 1.34±0.22 vs 0.85±0.17; p<0.001) and myocardium of healthy volunteers (TBRmean 1.34±0.22 vs 0.70±0.03; p<0.001). There was no 18F-fluciclatide uptake at sites of established prior infarction in patients with CTO, with activity similar to the myocardium of healthy volunteers (TBRmean 0.71±0.06 vs 0.70±0.03, p=0.83). 18F-Fluciclatide uptake occurred at sites of regional wall hypokinesia (wall motion index≥1 vs 0; TBRmean 0.93±0.31 vs 0.80±0.26 respectively, p<0.001) and subendocardial infarction. Importantly, although there was no correlation with infarct size (r=0.03, p=0.90) or inflammation (C reactive protein, r=-0.20, p=0.38), 18F-fluciclatide uptake was increased in segments displaying functional recovery (TBRmean 0.95±0.33 vs 0.81±0.27, p=0.002) and associated with increase in probability of regional recovery. CONCLUSION: 18F-Fluciclatide uptake is increased at sites of recent MI acting as a biomarker of cardiac repair and predicting regions of recovery. TRIAL REGISTRATION NUMBER: NCT01813045; Post-results.

The Value of Lead aVR ST Segment Changes in Localizing Culprit Lesion in Acute Inferior Myocardial Infarction and Its Prognostic Impact.

BACKGROUND: Identifying infarct-related artery (IRA) in patients with inferior ST elevation myocardial infarction (STEMI) has prognostic and therapeutic benefits. OBJECTIVES: To differentiate IRA and the location of culprit lesion in inferior STEMI, using ST segment changes in lead aVR. METHODS: ST segment changes in lead aVR were recorded in 150 patients, admitted with first inferior STEMI. The association of IRA and the location of culprit lesion with ST segment changes in aVR were investigated. RESULTS: ST elevation ≥ 0.5 mm in lead aVR was present in 17 patients (11.3%), ST depression ≥ 0.5 mm in 74 patients (49.3%) and 59 patients (39.3%) did not have significant ST segment changes. Right coronary artery (RCA) was the IRA in 117 patients (78%) and left circumflex artery (LCX) in 33 patients (22%). Prevalence of RCA involvement as the IRA was different in three study groups (94.1% in ST elevation group, 83.1% in isoelectric group and 70.3% in ST depression group, P = 0.049). Presence of ST elevation had a sensitivity and specificity of 13.68 % and 96.97%, for detecting RCA lesions, respectively. ST depression had 66.67% sensitivity and 55.56% specificity for identifying LCX lesions. Clinical complications were low in our study with no significant difference among patients of three groups. CONCLUSIONS: Presence of ST elevation is highly suggestive of RCA lesions versus LCX lesions, whereas absence of ST elevation cannot rule out RCA lesions. Presence of ST depression has a moderate sensitivity and specificity for LCX lesions.

Echocardiographic assessment of global longitudinal right ventricular function in patients with an acute inferior ST elevation myocardial infarction and proximal right coronary artery occlusion.

Right ventricular (RV) myocardial infarction (MI) is a frequent concomitant of an acute inferior MI. We set out to determine the diagnostic value of speckle tracking echocardiography in comparison with cardiac magnetic resonance (CMR) for RV stunning and scar prediction. 55 patients (66 ± 11 years) with an acute inferior ST elevation MI who underwent percutaneous coronary intervention (PCI) of an occlusion in the proximal right coronary artery were prospectively enrolled. An echocardiography was done on the day of presentation and on the 5th day thereafter. A CMR was subsequently performed 1 month after the MI. The CMR was used to differentiate between the group with RV scar (n = 26) and without RV scar (n = 29). RV peak systolic longitudinal strain (RV-LS) at presentation determined RV scar (-21.1 ± 5.1% vs. -9.9 ± 4.6%, p < 0.0001). The RV-LS correlated with the scar extent (r = 0.83, p < 0.0001). RV-LS > -15.8% had a sensitivity of 92% and a specificity of 83% in RV scar prediction (AUC 0.93). RV-LS was superior to TAPSE and TDI in determining the presence of RV scar. According to RV-LS values at presentation and on the 5th day, 3 subgroups were defined: G1-normal deformation (RV-LS <-20%), G2-RV stunning (baseline RV-LS >-20%, 5th day RV-LS <-20%) and G3-persistent RV dysfunction (unchanged RV-LS > -20%). In G1, there was neither RV scar nor clinically relevant hypotension. In G2, 58% of patients developed RV scar and 36% had hypotension. In the G3, 83% developed RV scar and 55% had hypotension. The myocardial deformation analysis could provide an early prediction of RV scar. It allowed the patients to be divided into subgroups with normal RV function, stunning and persistent RV dysfunction.

Microvascular obstruction complicating acute right ventricular myocardial infarction.

This case history describes a man with inferior myocardial infarction (MI) with right-ventricular involvement, treated with a right coronary artery stent. Magnetic resonance showed akinesia of left-ventricular inferior and inferolateral walls and right-ventricular inferior free wall with an impairment of global systolic function. There was late gadolinium enhancement (LGE) of left-ventricular inferior and inferolateral walls with microvascular obstruction (MVO). LGE of the right-ventricular inferior wall was seen with a hypointense core within hyperenhanced myocardium, consistent with MVO of the infarcted right-ventricular myocardium. At follow-up there was persistent akinesia of left-ventricular inferior and inferolateral walls and right-ventricular systolic dysfunction. LGE was still evident with resolution of MVO.

Mitral apparatus assessment by delayed enhancement CMR: relative impact of infarct distribution on mitral regurgitation.

OBJECTIVES: This study sought to assess patterns and functional consequences of mitral apparatus infarction after acute myocardial infarction (AMI). BACKGROUND: The mitral apparatus contains 2 myocardial components: papillary muscles and the adjacent left ventricular (LV) wall. Delayed-enhancement cardiac magnetic resonance (DE-CMR) enables in vivo study of inter-relationships and potential contributions of LV wall and papillary muscle infarction (PMI) to mitral regurgitation (MR). METHODS: Multimodality imaging was performed: CMR was used to assess mitral geometry and infarct pattern, including 3D DE-CMR for PMI. Echocardiography was used to measure MR. Imaging occurred 27 ± 8 days after AMI (CMR, echocardiography within 1 day). RESULTS: A total of 153 patients with first AMI were studied; PMI was present in 30% (n = 46 [72% posteromedial, 39% anterolateral]). When stratified by angiographic culprit vessel, PMI occurred in 65% of patients with left circumflex, 48% with right coronary, and only 14% of patients with left anterior descending infarctions (p <0.001). Patients with PMI had more advanced remodeling as measured by LV size and mitral annular diameter (p <0.05). Increased extent of PMI was accompanied by a stepwise increase in mean infarct transmurality within regional LV segments underlying each papillary muscle (p <0.001). Prevalence of lateral wall infarction was 3-fold higher among patients with PMI compared to patients without PMI (65% vs. 22%, p <0.001). Infarct distribution also impacted MR, with greater MR among patients with lateral wall infarction (p = 0.002). Conversely, MR severity did not differ on the basis of presence (p = 0.19) or extent (p = 0.12) of PMI, or by angiographic culprit vessel. In multivariable analysis, lateral wall infarct size (odds ratio 1.20/% LV myocardium [95% confidence interval: 1.05 to 1.39], p = 0.01) was independently associated with substantial (moderate or greater) MR even after controlling for mitral annular (odds ratio 1.22/mm [1.04 to 1.43], p = 0.01), and LV end-diastolic diameter (odds ratio 1.11/mm [0.99 to 1.23], p = 0.056). CONCLUSIONS: Papillary muscle infarction is common after AMI, affecting nearly one-third of patients. Extent of PMI parallels adjacent LV wall injury, with lateral infarction-rather than PMI-associated with increased severity of post-AMI MR.

Electrocardiographic Q-wave "remodeling" in reperfused ST-segment elevation myocardial infarction: validation study with CMR.

OBJECTIVES: The aim of this study was to evaluate the evolution in Q-wave expression during the first 5 years after a primary, successfully reperfused ST-segment elevation myocardial infarction (MI), using cardiac magnetic resonance (CMR) for infarct location, and to depict changes in infarct size and left ventricular remodeling over time. BACKGROUND: In the absence of QRS confounders, abnormal Q waves are usually diagnostic of myocardial necrosis. It is hypothesized that Q-wave regression after MI could be related to smaller infarct sizes. Late gadolinium enhancement accurately depicts MI of any age. METHODS: Forty-six MI patients underwent electrocardiography and CMR at 1 week (baseline), 4 months, 1 year, and 5 years post-infarction. Conventional CMR parameters were analyzed, and infarct presence, location, and size were assessed using late gadolinium enhancement CMR. Infarct locations were anterior or nonanterior (inferior and/or lateral), using late gadolinium enhancement CMR as a reference. For each time point, patients were classified as having a diagnostic/nondiagnostic electrocardiogram (ECG) using the European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation consensus criteria for previous Q-wave infarct. RESULTS: At baseline, 11 patients (23%) did not meet the criteria for Q-wave MI. Non-Q-wave infarcts were significantly smaller than Q-wave infarcts (p < 0.0001). All anterior Q-wave infarcts (n = 17) were correctly localized, whereas in 7 of 19 nonanterior Q-wave infarcts, the location or extent of the infarct was misjudged by electrocardiography. At 4-month/1-year follow-up, in 10 patients (3 anterior/7 nonanterior), the ECG became nondiagnostic. The ECG remained nondiagnostic at 5-year follow-up. A cutoff infarct size of 6.2% at 1 year yielded a sensitivity of 89% and a specificity of 74% to predict the presence or absence of Q waves. CONCLUSIONS: The incidence of nondiagnostic ECGs for previous MI using the current European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation criteria is substantial and increases with time post-infarction from 23% immediately post-infarction to 44% at 5-year follow-up.

[Deviation of ST-segment and detection of infarction related artery in patients with acute inferior wall infarction].

OBJECTIVE: To explore the characteristics of ST-segment deviation in patients with acute ST elevation myocardial infarction(STEMI)having only one vessel lesion in either left circumflex artery (LCX) or right coronary artery (RCA). METHODS: All AMI (acute myocardial infarction) patients were admitted into Peking Union Medical College Hospital from January 1996 to March 2009. They underwent coronary angiography (CAG). And the IRA (infarction-related artery) was either LCX or RCA without other coronary artery stenosis. Their ST-segments deviations on electrocardiogram (ECG) were analyzed quantitatively. RESULTS: Among 2503 AMI cases undergoing CAG during hospitalization, 75 cases had LCX (n = 16) or RCA (n = 59)-related STEMI. The RCA group was further divided into the proximal subgroup (n = 21) and the distal subgroup (n = 38). RCA as IRA was diagnosed when ST I depression < 0, ST V(1) elevation ≥ 0 or ST I and aVL depression < 0 with the sensitivities of 55.9%, 74.6% and 54.2% and the specificities of 81.3%, 62.5% and 81.3% respectively. LCX as IRA was diagnosed when ST aVR depression ≥ 0.1 mv, ST I elevation ≥ 0 or ST V(5) and V(6) elevation ≥ 0 with the sensitivities of 68.8%, 81.3% and 31.3% and the specificities of 76.3%, 59.3% and 91.5% respectively. Proximal occlusion of RCA was diagnosed when there was no ST depression in V(1) and depression in V(2), Max precordial ST depression in V(1)-V(3) with the sensitivities of 47.6% and 52.4% and the specificities of 78.9% and 84.2%. CONCLUSION: While discriminating IRA in STEMI patients with single LCX or RCA lesion, it is necessary to assess all ST-segments deviations on ECG.

A case with the longest angiographically documented left main coronary artery.

The left main coronary artery (LMC) is generally considered to be between 5 and 15 mm long. We report a case with the longest angiographically documented LMC (41 mm) in a patient with acute inferior myocardial infarction.

Relation of nausea and vomiting in acute myocardial infarction to location of the infarct.

To determine whether the incidence of nausea and vomiting in patients with acute myocardial infarction (AMI) varies with infarct location, we studied 180 patients who had been admitted to our hospital for ST-segment elevation AMI or AMI associated with left bundle branch block. The presenting symptoms (chest pain, nausea, and vomiting), initial electrocardiographic findings, and additional demographic, clinical, laboratory, and outcome data were extracted from the medical records and correlated with the infarct location. Of the 180 patients with AMI, 108 (60%) had inferior and 72 (40%) had anterior infarcts. Nausea was reported in almost 2/3 of all patients, and vomiting in nearly 1/3. Both nausea and vomiting showed a trend toward a greater incidence in patients with inferior than with anterior infarcts (69% vs 56% and 33% vs 26%, respectively). However, the differences were not statistically significant. In conclusion, nausea and vomiting are common presenting symptoms in patients with either inferior or anterior wall AMI, but their frequency is unrelated to the infarct location.