Jiwon Kim

Echocardiographic Algorithm for Post-Myocardial Infarction LV Thrombus: A Gatekeeper for Thrombus Evaluation by Delayed Enhancement CMR.

OBJECTIVESnThe goal of this study was to determine the prevalence of post-myocardial infarction (MI) left ventricular (LV) thrombus in the current era and to develop an effective algorithm (predicated on echocardiography [echo]) to discern patients warranting further testing for thrombus via delayed enhancement (DE) cardiac magnetic resonance (CMR).nnnBACKGROUNDnLV thrombus affects post-MI management. DE-CMR provides thrombus tissue characterization and is a well-validated but an impractical screening modality for all patients after an MI.nnnMETHODSnA same-day echo and CMR were performed according to a tailored protocol, which entailed uniform echo contrast (irrespective of image quality) and dedicated DE-CMR for thrombus tissue characterization.nnnRESULTSnA total of 201 patients were studied; 8% had thrombus according to DE-CMR. All thrombi were apically located; 94% of thrombi occurred in the context of a left anterior descending (LAD) infarct-related artery. Although patients with thrombus had more prolonged chest pain and larger MI (pxa0≤ 0.01), only 18% had aneurysm on echo (cine-CMR 24%). Noncontrast (35%) and contrast (64%) echo yielded limited sensitivity for thrombus on DE-CMR. Thrombus was associated with stepwise increments in basal → apical contractile dysfunction on echo and quantitative cine-CMR; the echo-measured apical wall motion score was higher among patients with thrombus (pxa0< 0.001) and paralleled cine-CMR decrements in apical ejection fraction and peak ejection rates (both pxa0< 0.005). Thrombus-associated decrements in apical contractile dysfunction were significant even among patients with LAD infarction (pxa0<xa00.05). The echo-based apical wall motion score improved overall performance (area under the curve 0.89xa0± 0.44) for thrombus compared with ejection fraction (area under the curve 0.80 ± 0.61; pxa0= 0.01). Apical wall motion partitions would have enabled all patients with LV thrombus to be appropriately referred for DE-CMR testing (100% sensitivity and negative predictive value), while avoiding further testing in more than one-half (56% to 63%) of patients.nnnCONCLUSIONSnLV thrombus remains common, especially after LAD MI, and can occur even in the absence of aneurysm. Although DE-CMR yielded improved overall thrombus detection, apical wall motion on a noncontrast echocardiogram canxa0be an effective stratification tool to identify patients in whom DE-CMR thrombus assessment is most warranted. (Diagnostic Utility of Contrast Echocardiography for Detection of LV Thrombi Post ST Elevation Myocardial Infarction; NCT00539045).

Effect of Myocardial Perfusion Pattern on Frequency and Severity of Mitral Regurgitation in Patients With Known or Suspected Coronary Artery Disease

Mitral regurgitation (MR) is common with coronary artery disease as altered myocardial substrate can affect valve performance. Single-photon emission computed tomography myocardial perfusion imaging (MPI) enables assessment of myocardial perfusion alterations. This study examined perfusion pattern in relation to MR. A total of 2,377 consecutive patients with known or suspected coronary artery disease underwent stress MPI and echocardiography within 1.6 ± 2.3xa0days. MR was present on echocardiography in 34% of patients, among whom 13% had advanced (moderate or more) MR. MR prevalence was higher in patients with abnormal MPI (44% vs 29%, p <0.001), corresponding to increased global ischemia (p <0.001). Regional perfusion varied in left ventricular segments adjacent to each papillary muscle: adjacent to the anterolateral papillary muscle, magnitude of baseline and stress-induced anterior/anterolateral perfusion abnormalities was greater in patients with MR (both p <0.001). Adjacent to the posteromedial papillary muscle, baseline inferior/inferolateral perfusion abnormalities were greater with MR (p <0.001), whereas stress inducibility was similar (pxa0= 0.39). In multivariate analysis, stress-induced anterior/anterolateral and rest inferior/inferolateral perfusion abnormalities were independently associated with MR (both p <0.05) even after controlling for perfusion in reference segments not adjacent to the papillary muscles. MR severity increased in relation to magnitude of perfusion abnormalities in each territory adjacent to the papillary muscles, as evidenced by greater prevalence of advanced MR in patients with at least moderate anterior/anterolateral stress perfusion abnormalities (10.7% vs 3.6%), with similar results when MR was stratified based on rest inferior/inferolateral perfusion (10.4% vs 3.0%, both p <0.001). In conclusion, findings demonstrate that myocardial perfusion pattern in left ventricular segments adjacent to the papillary muscles influences presence and severity of MR.

Use of High-Sensitivity Troponin Assays Predicts Mortality in Patients With Normal Conventional Troponin Assays on Admission—Insights From a Meta-Analysis

Use of high‐sensitivity troponin (hs‐Tn) assays can detect small levels of myocardial damage previously undetectable with conventional troponin (c‐Tn) assays. However, prognostic utility of these hs‐Tn assays in prediction of mortality remains unclear in the presence of nonelevated c‐Tn levels on admission. A systematic review and meta‐analysis was performed to assess mortality risk of patients with hs‐Tn elevations in the setting of normal c‐Tn levels.

Echocardiographic Linear Dimensions for Assessment of Right Ventricular Chamber Volume as Demonstrated by Cardiac Magnetic Resonance

BACKGROUNDnEchocardiography-derived linear dimensions offer straightforward indices of right ventricular (RV) structure but have not been systematically compared with RV volumes on cardiac magnetic resonance (CMR).nnnMETHODSnEchocardiography and CMR were interpreted among patients with coronary artery disease imaged via prospective (90%) and retrospective (10%) registries. For echocardiography, American Society of Echocardiography-recommended RV dimensions were measured in apical four-chamber (basal RV width, mid RV width, and RV length), parasternal long-axis (proximal RV outflow tract [RVOT]), and short-axis (distal RVOT) views. For CMR, RV end-diastolic volume and RV end-systolic volume were quantified using border planimetry.nnnRESULTSnTwo hundred seventy-two patients underwent echocardiography and CMR within a narrow interval (0.4xa0±xa01.0xa0days); complete acquisition of all American Society of Echocardiography-recommended dimensions was feasible in 98%. All echocardiographic dimensions differed between patients with and those without RV dilation on CMR (Pxa0<xa0.05). Basal RV width (rxa0=xa00.70), proximal RVOT width (rxa0=xa00.68), and RV length (rxa0=xa00.61) yielded the highest correlations with RV end-diastolic volume on CMR; end-systolic dimensions yielded similar correlations (rxa0=xa00.68, rxa0=xa00.66, and rxa0=xa00.65, respectively). In multivariate regression, basal RV width (regression coefficientxa0=xa01.96 per mm; 95% CI, 1.22-2.70; Pxa0<xa0.001), RV length (regression coefficientxa0=xa00.97; 95% CI, 0.56-1.37; Pxa0<xa0.001), and proximal RVOT width (regression coefficientxa0=xa02.62; 95% CI, 1.79-3.44; Pxa0<xa0.001) were independently associated with CMR RV end-diastolic volume (rxa0=xa00.80). RV end-systolic volume was similarly associated with echocardiographic dimensions (basal RV width: 1.59 per mm [95% CI, 1.06-2.13], Pxa0<xa0.001; RV length: 1.00 [95% CI, 0.66-1.34], Pxa0<xa0.001; proximal RVOT width: 1.80 [95% CI, 1.22-2.39], Pxa0<xa0.001) (rxa0=xa00.79).nnnCONCLUSIONSnRV linear dimensions provide readily obtainable markers of RV chamber size. Proximal RVOT and basal width are independently associated with CMR volumes, supporting the use of multiple linear dimensions when assessing RV size on echocardiography.

Association of Right Ventricular Pressure and Volume Overload with Non-Ischemic Septal Fibrosis on Cardiac Magnetic Resonance

Background Non-ischemic fibrosis (NIF) on cardiac magnetic resonance (CMR) has been linked to poor prognosis, but its association with adverse right ventricular (RV) remodeling is unknown. This study examined a broad cohort of patients with RV dysfunction, so as to identify relationships between NIF and RV remodeling indices, including RV pressure load, volume and wall stress. Methods and Results The population comprised patients with RV dysfunction (EF<50%) undergoing CMR and transthoracic echo within a 14 day (5±3) interval. Cardiac structure, function, and NIF were assessed on CMR. Pulmonary artery systolic pressure (PASP) was measured on echo. 118 patients with RV dysfunction were studied, among whom 47% had NIF. Patients with NIF had lower RVEF (34±10 vs. 39±9%; p = 0.01) but similar LVEF (40±21 vs. 39±18%; p = 0.7) and LV volumes (p = NS). RV wall stress was higher with NIF (17±7 vs. 12±6 kPa; p<0.001) corresponding to increased RV end-systolic volume (143±79 vs. 110±36 ml; p = 0.006), myocardial mass (60±21 vs. 53±17 gm; p = 0.04), and PASP (52±18 vs. 41±18 mmHg; p = 0.001). NIF was associated with increased wall stress among subgroups with isolated RV (p = 0.005) and both RV and LV dysfunction (p = 0.003). In multivariable analysis, NIF was independently associated with RV volume (OR = 1.17 per 10 ml, [CI 1.04–1.32]; p = 0.01) and PASP (OR = 1.43 per 10 mmHg, [1.14–1.81]; p = 0.002) but not RV mass (OR = 0.91 per 10 gm, [0.69–1.20]; p = 0.5) [model χ2 = 21; p<0.001]. NIF prevalence was higher in relation to PA pressure and RV dilation and was > 6-fold more common in the highest, vs. the lowest, common tertile of PASP and RV size (p<0.001). Conclusion Among wall stress components, NIF was independently associated with RV chamber dilation and afterload, supporting the concept that NIF is linked to adverse RV chamber remodeling.

Right Ventricular Dysfunction Impairs Effort Tolerance Independent of Left Ventricular Function Among Patients Undergoing Exercise Stress Myocardial Perfusion ImagingCLINICAL PERSPECTIVE

Background—Right ventricular (RV) and left ventricular (LV) function are closely linked due to a variety of factors, including common coronary blood supply. Altered LV perfusion holds the potential to affect the RV, but links between LV ischemia and RV performance, and independent impact of RV dysfunction on effort tolerance, are unknown. Methods and Results—The population comprised 2051 patients who underwent exercise stress myocardial perfusion imaging and echo (5.5±7.9 days), among whom 6% had echo-evidenced RV dysfunction. Global summed stress scores were ≈3-fold higher among patients with RV dysfunction, attributable to increments in inducible and fixed LV perfusion defects (all P⩽0.001). Regional inferior and lateral wall ischemia was greater among patients with RV dysfunction (both P<0.01), without difference in corresponding anterior defects (P=0.13). In multivariable analysis, inducible inferior and lateral wall perfusion defects increased the likelihood of RV dysfunction (both P<0.05) independent of LV function, fixed perfusion defects, and pulmonary artery pressure. Patients with RV dysfunction demonstrated lesser effort tolerance whether measured by exercise duration (6.7±2.8 versus 7.9±2.9 minutes; P<0.001) or peak treadmill stage (2.6±0.9 versus 3.1±1.0; P<0.001), paralleling results among patients with LV dysfunction (7.0±2.9 versus 8.0±2.9; P<0.001|2.7±1.0 versus 3.1±1.0; P<0.001 respectively). Exercise time decreased stepwise in relation to both RV and LV dysfunction (P<0.001) and was associated with each parameter independent of age or medication regimen. Conclusions—Among patients with known or suspected coronary artery disease, regional LV ischemia involving the inferior and lateral walls confers increased likelihood of RV dysfunction. RV dysfunction impairs exercise tolerance independent of LV dysfunction.

P wave area for quantitative electrocardiographic assessment of left atrial remodeling.

Background Left atrial (LA) dilation provides a substrate for mitral regurgitation (MR) and atrial arrhythmias. ECG can screen for LA dilation but standard approaches do not assess LA geometry as a continuum, as does non-invasive imaging. This study tested ECG-quantified P wave area as an index of LA geometry. Methods and Results 342 patients with CAD underwent ECG and CMR within 7 (0.1±1.4) days. LA area on CMR correlated best with P wave area in ECG lead V1 (ru200a=u200a0.42, p<0.001), with lesser correlations for P wave amplitude and duration. P wave area increased stepwise in relation to CMR-evidenced MR severity (p<0.001), with similar results for MR on echocardiography (performed in 86% of patients). Pulmonary arterial (PA) pressure on echo was increased by 50% among patients in the highest (45±14 mmHg) vs. the lowest (31±9 mmHg) P wave area quartile of the population. In multivariate regression, CMR and echo-specific models demonstrated P wave area to be independently associated with LA size after controlling for MR, as well as echo-evidenced PA pressure. Clinical follow-up (mean 2.4±1.9 years) demonstrated ECG and CMR to yield similar results for stratification of arrhythmic risk, with a 2.6-fold increase in risk for atrial fibrillation/flutter among patients in the top P wave area quartile of the population (CI 1.1–5.9, pu200a=u200a0.02), and a 3.2-fold increase among patients in the top LA area quartile (CI 1.4–7.0, pu200a=u200a0.005). Conclusions ECG-quantified P wave area provides an index of LA remodeling that parallels CMR-evidenced LA chamber geometry, and provides similar predictive value for stratification of atrial arrhythmic risk.

Left ventricular geometric remodeling in relation to non-ischemic scar pattern on cardiac magnetic resonance imaging

Left ventricular (LV) remodeling and myocardial fibrosis have been linked to adverse heart failure outcomes. Mid wall late gadolinium enhancement (MW-LGE) on cardiac magnetic resonance (CMR) imaging is well-associated with non-ischemic cardiomyopathy (NICM), but prevalence in ischemic cardiomyopathy (ICM) and association with remodeling are unknown. The population comprised patients with systolic dysfunction [LV ejection fraction (LVEFxa0≤xa040xa0%)]. CMR was used to identify MW-LGE, conventionally defined as fibrosis of the mid-myocardial or epicardial aspect of the LV septum. 285 patients were studied. MW-LGE was present in 12xa0%, and was tenfold more common with NICM (32xa0%) versus ICM (3xa0%, pxa0<xa00.001). However, owing to higher prevalence of ICM, 15xa0% of patients with MW-LGE had ICM. LV wall stress was higher (pxa0=xa00.02) among patients with, versus those without, MW-LGE despite similar systolic blood pressure (pxa0=xa00.24). In multivariate analysis, MW-LGE was associated with CMR-quantified LV end-diastolic volume (pxa0=xa00.03) independent of LVEF and mass. Incorporation of clinical and imaging variables demonstrated MW-LGE to be associated with higher LV end-diastolic volume (OR 1.13, CI 1.004–1.27 per 10xa0ml/m2, pxa0=xa00.04) after controlling for presence of NICM (OR 16.0, CI 5.8–44.1, pxa0<xa00.001). While more common in NICM, MW-LGE can occur in ICM and is a marker of LV chamber dilation irrespective of cardiomyopathic etiology.

Pattern and Prognostic Implications of Cardiac Metastases Among Patients With Advanced Systemic Cancer Assessed With Cardiac Magnetic Resonance Imaging.

Background Cardiac magnetic resonance (CMR) imaging is well validated for tissue characterization of cardiac masses but has not been applied to study pattern and prognostic implications of cardiac metastases (CMETs) among patients with systemic cancer. Methods and Results The population consisted of 60 patients with stage IV cancer (32 patients with CMETs, 28 diagnosis‐matched controls) undergoing CMR. CMET was defined as a discrete mass with vascular tissue properties on delayed enhancement CMR. CMET‐positive patients and controls had similar clinical characteristics, cardiac geometry, and function (P=NS). Leading cancer types associated with CMET were sarcoma, melanoma, and gastrointestinal. Patients with CMETs had similar distribution of extracardiac metastatic disease compared with controls (organs involved: 3.4±2.0 versus 2.7±1.9, P=0.17). In 94% of patients with CMETs, there were metastases involving ≥1 extracardiac organ (66% lung involvement). CMET location varied (right ventricle 44%, right atrium 19%, left ventricle 28%, left atrium 9%, pericardial 25%); 22% of cases had multichamber involvement. Right‐sided chamber involvement was common in hematologic/lymphatic spread (67%); pericardial involvement was common with direct spread (64%). Regarding tissue properties on delayed enhancement CMR, CMETs commonly (59%) demonstrated heterogeneous enhancement (41% diffuse enhancement). Heterogeneous lesions were larger and had increased border irregularity (P<0.05). Survival 6 months post‐CMR was numerically lower among patients with CMETs (56% [95% CI 39–74%]) versus stage IV cancer–matched controls (68% [95% CI 50–86%]), although differences between groups were nonsignificant (P=0.42). Conclusions CMETs vary regarding etiology, location, and tissue properties on CMR, highlighting need for comprehensive surveillance of cardiac involvement regardless of cancer origin. Prognosis remains poor with for patients with CMETs, albeit similar to that for stage IV cancer controls matched for cancer etiology.

Prognostic utility of differential tissue characterization of cardiac neoplasm and thrombus via late gadolinium enhancement cardiovascular magnetic resonance among patients with advanced systemic cancer

BackgroundLate gadolinium enhancement (LGE-) cardiovascular magnetic resonance (CMR) is well-validated for cardiac mass (CMASS) tissue characterization to differentiate neoplasm (CNEO) from thrombus (CTHR): Prognostic implications of CMASS subtypes among systemic cancer patients are unknown.MethodsCMASSxa0+xa0patients and controls (CMASS -) matched for cancer diagnosis and stage underwent a standardized CMR protocol, including LGE-CMR (IR-GRE) for tissue characterization and balanced steady state free precession cine-CMR (SSFP) for cardiac structure/function. CMASS subtypes (CNEO, CTHR) were respectively defined by presence or absence of enhancement on LGE-CMR; lesions were quantified for tissue properties (contrast-to-noise ratio (CNR); signal-to-noise ratio (SNR) and size. Clinical follow-up was performed to evaluate prognosis in relation to CMASS etiology.ResultsThe study population comprised 126 patients with systemic neoplasms referred for CMR, of whom 50% (nxa0=xa063) had CMASS + (CNEOxa0=xa032%, CTHRxa0=xa018%). Cancer etiology differed between CNEO (sarcomaxa0=xa020%, lungxa0=xa018%) and CTHR (lymphomaxa0=xa030%, GIxa0=xa026%); cardiac function (left ventricular ejection fraction: 63xa0±xa09 vs. 62xa0±xa010%; pxa0=xa00.51∣ right ventricular ejection fraction: 53xa0±xa09 vs. 54xa0±xa08%; pxa0=xa00.47) and geometric indices were similar (all pxa0=xa0NS). LGE-CMR tissue properties assessed by CNR (13.1xa0±xa013.0 vs. 1.6xa0±xa01.0; pxa0<xa00.001) and SNR (29.7xa0±xa020.4 vs. 15.0xa0±xa011.4, pxa0=xa00.003) were higher for CNEO, consistent with visually-assigned diagnostic categories. CTHR were more likely to localize to the right atrium (78% vs. 25%, pxa0<xa00.001); nearly all (17/18) were associated with central catheters. Lesion size (17.3xa0±xa023.8 vs. 2.0xa0±xa01.5xa0cm2; pxa0<xa00.001) was greater with CNEO vs. CTHR, as was systemic disease burden (cancer-involved organs: 3.6xa0±xa02.0 vs. 2.3xa0±xa02.1; pxa0=xa00.02). Mortality during a median follow-up of 2.5xa0years was markedly higher among patients with CNEO compared to those with CTHR (HRxa0=xa03.13 [CI 1.54–6.39], pxa0=xa00.002); prognosis was similar when patients were stratified by lesion size assessed via area (HRxa0=xa00.99 per cm2 [CI 0.98–1.01], pxa0=xa00.40) or maximal diameter (HRxa0=xa00.98 per cm [CI 0.91–1.06], pxa0=xa00.61). CTHR conferred similar mortality risk compared to cancer-matched controls without cardiac involvement (pxa0=xa00.64) whereas mortality associated with CNEO was slightly higher albeit non-significant (pxa0=xa00.12).ConclusionsAmong a broad cancer cohort with cardiac masses, CNEO defined by LGE-CMR tissue characterization conferred markedly poorer prognosis than CTHR, whereas anatomic assessment via cine-CMR did not stratify mortality risk. Both CNEO and CTHR are associated with similar prognosis compared to CMASS - controls matched for cancer type and disease extent.