Artificial Intelligence-Enabled Quantitative Coronary Plaque and Hemodynamic Analysis for Predicting Acute Coronary Syndrome.

BACKGROUND: A lesion-level risk prediction for acute coronary syndrome (ACS) needs better characterization. OBJECTIVES: This study sought to investigate the additive value of artificial intelligence-enabled quantitative coronary plaque and hemodynamic analysis (AI-QCPHA). METHODS: Among ACS patients who underwent coronary computed tomography angiography (CTA) from 1 month to 3 years before the ACS event, culprit and nonculprit lesions on coronary CTA were adjudicated based on invasive coronary angiography. The primary endpoint was the predictability of the risk models for ACS culprit lesions. The reference model included the Coronary Artery Disease Reporting and Data System, a standardized classification for stenosis severity, and high-risk plaque, defined as lesions with ≥2 adverse plaque characteristics. The new prediction model was the reference model plus AI-QCPHA features, selected by hierarchical clustering and information gain in the derivation cohort. The model performance was assessed in the validation cohort. RESULTS: Among 351 patients (age: 65.9 ± 11.7 years) with 2,088 nonculprit and 363 culprit lesions, the median interval from coronary CTA to ACS event was 375 days (Q1-Q3: 95-645 days), and 223 patients (63.5%) presented with myocardial infarction. In the derivation cohort (n = 243), the best AI-QCPHA features were fractional flow reserve across the lesion, plaque burden, total plaque volume, low-attenuation plaque volume, and averaged percent total myocardial blood flow. The addition of AI-QCPHA features showed higher predictability than the reference model in the validation cohort (n = 108) (AUC: 0.84 vs 0.78; P < 0.001). The additive value of AI-QCPHA features was consistent across different timepoints from coronary CTA. CONCLUSIONS: AI-enabled plaque and hemodynamic quantification enhanced the predictability for ACS culprit lesions over the conventional coronary CTA analysis. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary Computed Tomography Angiography and Computational Fluid Dynamics II [EMERALD-II]; NCT03591328).

Diagnostic and Clinical Value of FFRCT in Stable Chest Pain Patients With Extensive Coronary Calcification: The FACC Study.

BACKGROUND: The influence of extensive coronary calcifications on the diagnostic and prognostic value of coronary computed tomography angiography-derived fractional flow reserve (FFRCT) has been scantily investigated. OBJECTIVES: The purpose of this study was to investigate the diagnostic and short-term role of FFRCT in chest pain patients with Agatston score (AS) >399. METHODS: This was a prospective multicenter study of 260 stable patients with suspected coronary artery disease (CAD) and AS >399. FFRCT was measured blinded by an independent core laboratory. All patients underwent invasive coronary angiography (ICA) and FFR if indicated. The agreement of FFRCT ≤0.80 with hemodynamically significant CAD on ICA/FFR (≥50% left main or ≥70% epicardial artery stenosis and/or FFR ≤0.80) was assessed. Patients undergoing FFR had colocation FFRCT measured, and the lowest per-patient FFRCT was registered in all patients. The association among per-patient FFRCT, coronary revascularization, and major clinical events (all-cause mortality, myocardial infarction, or unstable angina hospitalization) at 90-day follow-up was evaluated. RESULTS: Median age and AS were 68.5 years (IQR: 63-74 years) and 895 (IQR: 587-1,513), respectively. FFRCT was ≤0.80 in 204 patients (78%). Colocation FFRCT (n = 112) showed diagnostic accuracy, sensitivity, and specificity to identify hemodynamically significant CAD of 71%, 87%, and 54%. The area under the receiver-operating characteristics curve (AUC) was 0.75. When using the lowest FFRCT (n = 260), per-patient accuracy, sensitivity, and specificity were 57%, 95%, and 32%, respectively. The AUC was 0.84. A total of 85 patients underwent revascularization, and FFRCT was ≤0.80 in 96% of these. During follow-up, major clinical events occurred in 3 patients (1.2%), all with FFRCT ≤0.80. CONCLUSIONS: Most patients with AS >399 had FFRCT ≤0.80. Using ICA/FFR as the reference revealed a moderate diagnostic accuracy of colocation FFRCT. Compared with the lowest per-patient FFRCT, colocation FFRCT measurement improved diagnostic accuracy and specificity. The 90-day follow-up was favorable with few coronary revascularizations and no major clinical events occurring in patients with FFRCT >0.80. (Use of FFR-CT in Stable Intermediate Chest Pain Patients With Severe Coronary Calcium Score [FACC]; NCT03548753).

Anti-Neutrophil Cytoplasmic Antibody (ANCA) Associated Vasculitis Causes Aortic Valve Degeneration and Severe Aortic Regurgitation.

BACKGROUND Granulomatosis with polyangiitis (GPA)/Wegener's granulomatosis (WG) and eosinophilic granulomatosis with polyangiitis (EGPA)/Churg-Strauss' syndrome (CSS) are ANCA (antineutrophil cytoplasmic antibodies) associated vasculitides that can affect the heart, predominantly the myocardium. Valvular affection is rare and is described anecdotally. The purpose of this case report was to present aortic valve affection of an ANCA positive vasculitis. CASE REPORT We present the case with a 56-year-old male diagnosed with ANCA associated vasculitis, who began experiencing respiratory symptoms primarily thought to be respiratory tract affection. These symptoms worsened, and an echocardiography revealed heart failure with decreased left ventricular ejections fraction (EF=30-35%) and a severe insufficiency of the aortic valve. The patient underwent aortic valve replacement with symptomatic relief. Pathological examination of aortic valve resectates revealed inflammation and thickening of the aortic cusps. CONCLUSIONS Patients with ANCA associated vasculitis can rarely present with valvular inflammation causing severe regurgitation. The aortic valve can be involved, although cases have also described mitral valve involvement and both valves simultaneously. In patients with ANCA associated vasculitis a severe worsening of dyspnea can be caused by exacerbation of pulmonary involvement, but severe valvular disease should also be considered.

Impact of a motion correction algorithm on image quality in patients undergoing CT angiography: A randomized controlled trial.

AIMS: To investigate the motion correction algorithm Snapshot-Freeze (SSF) compared to standard reconstruction (STD) in patients randomized to receive beta-blockers (BB) or no beta-blockers (non-BB) before coronary CT, and to investigate if SSF can replace BB. METHODS: One hundred and forty patients scheduled for coronary CT were randomized. All images were reconstructed by the SSF and STD algorithms. Image quality was evaluated according to Likert score (1: excellent, 2: good, 3: adequate, 4: non-diagnostic) and presence of artifacts was noted. RESULTS: Images from 64 patients in the BB group (mean HR 56±4bpm) and 51 patients in the non-BB group (mean HR 67±7bpm) were analyzed. Twenty five patients were excluded because of tachycardia, bradycardia or reconstruction errors in SSF. SSF increased the number of excellent images in both groups compared to the STD algorithm (BB: 59% vs.44%; non-BB: 25% vs. 8%), but the number of non-diagnostic images was not significantly reduced. SSF reduced motion artifacts (BB: 11% vs. 31%; non-BB: 49% vs. 75%), but despite this reduction, motion artifacts in non-BB were still more frequent compared to the BB group analyzed by STD (49% vs. 31%). CONCLUSION: SSF improves image quality and reduces motion artifacts, but does not compensate for the absence of BB.

Impact of a motion correction algorithm on quality and diagnostic utility in unselected patients undergoing coronary CT angiography.

AIMS: The aims of the study were to investigate the diagnostic utility of motion correction reconstruction algorithm Snapshot Freeze (SSF) compared to the standard reconstruction algorithm (STD) in coronary computed tomography angiography (CCTA) images where a prescan heart-rate-lowering protocol is fully integrated. METHODS: CCTA was performed in 140 patients. Two independent blinded readers made image evaluation of the SSF and STD images. RESULTS: SSF reduced the motion artifacts (30% vs. 41%; P<.05) and improved the image quality ("excellent" images: 52% vs. 42%; P=.022), but did not influence diagnostic utility ("nondiagnostic" images: 10% vs. 14%; P=.104). CONCLUSION: The use of the SSF algorithm reduced the presence of motion artifacts and improved image quality, but did not influence the diagnostic utility.

Diastolic wall motion abnormality after myocardial infarction: relation to neurohormonal activation and prognostic implications.

BACKGROUND: Systolic wall motion abnormality (WMA) after acute myocardial infarction (AMI) is a major determinant of outcome; the presence and importance of diastolic WMA after AMI are unknown. We therefore sought to detect diastolic WMA using color kinesis and to assess its relation to neurohormonal activation and its prognostic importance in a consecutive population with a first AMI. METHODS: Complete color-encoded color kinesis and 2-dimensional and Doppler echocardiography were performed in 149 consecutive patients with documented first AMI within 24 hours of their admission. N-terminal pro-brain natriuretic peptide was measured 3 days after AMI. Study end point was cardiac death or readmission for heart failure. RESULTS: Diastolic area of WMA exceeded the systolic area in all but 5 patients (97%) and was significantly correlated with brain natriuretic peptide (unadjusted beta = .67, P < .0001; adjusted for systolic function, age, Killip class, and overall diastolic function beta = .27, P = .007). Diastolic WMA was also correlated with the number of diseased vessels on coronary angiography (beta = .59, P < .0001). During follow-up, 25 patients died and 11 were readmitted because of recurrent heart failure. On univariate analysis, the area of diastolic WMA was a predictor of the composite end point (hazard ratio 1.07 [95% CI 1.05-1.09], P < .0001) and remained a predictor on multivariate Cox analysis after adjustment of well-known risk factors, left ventricular systolic and overall diastolic functions (hazard ratio 1.09 [95% CI 1.06-1.15], P < .001). CONCLUSION: The extent of diastolic WMA can be assessed early after AMI using color kinesis. Diastolic WMA is associated with neurohormonal activation and angiographic severity of coronary artery disease and provides independent prognostic information.

The Doppler myocardial performance index during low-dose dobutamine echocardiography predicts mortality and left ventricular dilation after a first acute myocardial infarction.

BACKGROUND: Myocardial viability can be detected by wall motion analysis during low-dose dobutamine echocardiography (LDDE) after acute myocardial infarction (AMI). However, wall motion analysis describes only left ventricular (LV) systolic reserve. The Doppler myocardial performance index (MPI) is a quantitative measure of combined LV systolic and diastolic function. We hypothesized that an increase (deterioration) in MPI during LDDE, reflecting reduced systolic and diastolic LV reserve, could provide prognostic information beyond conventional systolic wall motion analysis on mortality, morbidity, and LV remodeling after AMI. METHODS: Low-dose dobutamine echocardiography (10 microg/kg per minute) was performed within 24 hours and echocardiography was repeated 5 days and 1, 3, and 6 months after a first AMI in 162 consecutive patients. Patients were followed for 25 +/- 11 months. End points were all-cause mortality and cardiac events (cardiac death or readmission for heart failure or reinfarction). RESULTS: In 72 (44%) patients, MPI increased during LDDE. This was independently associated with subsequent LV dilation at 6 months of follow-up (beta = .73, P < .0001). An increase in MPI during LDDE was a powerful prognostic indicator and remained a predictor of mortality (HR 1.92, 95% CI 1.36-2.71, P < .0001) and cardiac events (HR 2.45, 95% CI 1.83-3.27, P < .0001) after adjustment for clinical data, indices of LV function at rest, and wall motion analysis during LDDE. CONCLUSIONS: Early after AMI, deterioration in MPI during LDDE predicts subsequent LV dilation and provides prognostic information incremental to clinical data, indices of LV function at rest, and conventional stress echocardiographic data.

Usefulness of left ventricular diastolic wall motion abnormality as an early predictor of left ventricular dilation after a first acute myocardial infarction.

To determine the relation between regional diastolic wall motion abnormality and left ventricular remodeling after acute myocardial infarction (AMI), Doppler echocardiography and color kinesis with assessment of global and regional systolic and diastolic functions were performed in 84 patients who developed AMI within 24 hours of admission. In a multivariate logistic regression analysis, the percentage of left ventricular myocardial segments with diastolic wall motion abnormality (p = 0.008), absence of myocardial viability (p = 0.01), and overall diastolic function (p = 0.001) were predictors of remodeling after AMI.

The myocardial performance index during low-dose dobutamine echocardiography in control subjects and patients with a recent myocardial infarction: a new index of left ventricular functional reserve?

BACKGROUND: Wall-motion analysis during low-dose dobutamine echocardiography (LDDE) is a semiquantitative measure of left ventricular contractile reserve after myocardial infarction (MI). The Doppler echocardiographic myocardial performance index (MPI) is a quantitative measure of combined left ventricular systolic and diastolic function. We sought to characterize the changes in MPI during LDDE in control subjects and patients with MI, and to describe the relation of these changes to changes in regional systolic function. METHODS: MPI was obtained at rest and during LDDE (10 microg/kg/min) in 25 healthy volunteers (group 1) and 50 patients with a recent MI. Patients were divided into two subsets; those with (n = 23; group 2A) and those without (n = 27; group 2B) a contractile reserve defined as an improvement of wall motion in more than two contiguous infarct-zone segments during LDDE. DeltaMPI was defined as the change from rest to LDDE. RESULTS: MPI decreased significantly during LDDE in groups 1 and 2A, whereas MPI increased in group 2B (DeltaMPI = 0.12 +/- 0.04 and 0.10 +/- 0.08 vs -0.03 +/- 0.08, P <.0001). On multivariate analysis, Deltawall-motion score index predicted DeltaMPI (beta = 0.65, P <.0001) independently of age, sex, and the dobutamine-induced change in heart rate and systolic blood pressure. CONCLUSIONS: Data suggest that the change in MPI during LDDE may provide a simple and quantitative measure of overall left ventricular functional reserve in patients with a recent MI.

Serial changes in regional diastolic left ventricular function after a first acute myocardial infraction.

After acute myocardial infarction (AMI), regional diastolic function may be abnormal even though regional systolic function appears normal. However, it is not known whether this represents a transient or permanent phenomenon, and the relation to myocardial viability is not known. To determine this we assessed regional left ventricular function during contraction and filling after AMI in 106 patients with a first AMI. Echocardiography with color kinesis was performed on day 1 and 1, 3, and 6 months after AMI. For both left ventricular systole and diastole the percentage of segments with abnormal wall motion was calculated. During the first 6 months, the area of diastolic wall-motion abnormality decreased (38 +/- 16%-30 +/- 27%, P = .001) whereas no overall change in area of systolic wall-motion abnormality was seen (18 +/- 15%-19 +/- 19%, P = .66). However, for patients with no viable myocardium no significant change in diastolic wall-motion abnormality occurred (baseline 45 +/- 12% vs 44 +/- 27% at 6 months, P = .93). In contrast, a significant decrease was seen for patients with viability (33 +/- 16%-22 +/- 23%, P < .001). This was almost exclusively caused by normalization of regions where only diastolic wall-motion abnormalities were present (19 +/- 11%-7 +/- 15%, P < .0001). In a multivariable regression model, myocardial viability (P = .01) and N-terminal pro-brain natriuretic peptide concentration on day 3 (P = .003) were associated with changes in regional diastolic wall-motion abnormalities. Thus, abnormal diastolic wall motion during diastole is frequently present after AMI, and it seems to resolve to a greater extent than abnormal systolic wall-motion abnormality especially for patients with myocardial viability. This suggests diastolic stunning.

Relation of early changes of QT dispersion to changes in left ventricular systolic and diastolic function after a first acute myocardial infarction.

OBJECTIVE: To describe the relation between changes of left ventricular systolic and diastolic function and changes of QT dispersion (difference in duration between longest and shortest QT interval) following acute myocardial infarction. DESIGN: QT dispersion was determined at admission, hospital discharge, and 1 and 3 months following myocardial infarction in 64 consecutive 1-year survivors. Patients were divided into Group A where QT dispersion was < 52 ms at all recordings or initially > 52 ms but decreased during follow-up, and Group B where QT dispersion remained increased > or = 52 ms at all measurements. Doppler-Echocardiography was carried out on day 1, day 5, and after 1, 3, and 12 months. RESULTS: In 26 patients QT dispersion remained increased > or = 52 ms during the first 3 months after infarction. Among these a significant increase of end-systolic volume was seen whereas low or rapid normalized QT dispersion was associated with a significant decrease of ventricular volumes. After 1 year end-systolic (70 +/- 32 ml vs 49 +/- 16 ml, p = 0.006) and end-diastolic volumes (138 +/- 41 ml vs 105 +/- 22 ml, p = 0.001) were higher in Group B. In a multivariate model Group B was significantly related to an increase of end-diastolic volume (p = 0.01). In Group A diastolic function improved in eight patients and in two it deteriorated, whereas improvement was seen in one patient and deterioration in nine patients from Group B (p < 0.01). CONCLUSION: Following myocardial infarction low QT dispersion is associated with preserved left ventricular function, whereas persistently increased dispersion is associated with left ventricular dilation and deterioration of diastolic function.