What is the Diagnostic Utility of Cardiac Magnetic Resonance Imaging in Unselected Patients With Premature Ventricular Contractions and Nonsustained Ventricular Tachycardia?

Patients with non-ischemic systolic heart failure (HF) have increased risk of sudden cardiovascular death (SCD). The initiation and substrate for ventricular arrhythmias remains poorly understood. Our purpose was to describe the relationship between cardiac magnetic resonance (CMR) late gadolinium enhancement (LGE) and Holter recorded ventricular arrhythmic activity. Patients from the DANISH trial underwent a Holter-recording and a CMR-scan. The presence of non-sustained ventricular tachycardia (NSVT) and premature ventricular contractions (PVC) were examined in relation to presence and amount of LGE. Outcome measures were all-cause mortality and SCD. Overall, 180 patients were included. LGE was present in 86 (47%). NSVT occurred in 72 (40%), not different according to LGE status (p = 0.65). The amount of LGE was not correlated to the occurrence of NSVT (p = 0.40). The occurrence of couplet PVCs (p = 0.997), frequent PVCs (p = 0.12), PVCs in bigemini (p = 0.29), in trigemini (p = 0.26), or in quadrimini (p = 0.35) did not differ according to LGE status. LGE was significantly associated with risk of all-cause mortality (HR 2.14; 95% CI 1.05-4.37, p = 0.04). NSVT did not increase risk of all-cause mortality in either patients with LGE (HR 1.00; 95% CI 0.46-2.16, p = 0.996) or without LGE (HR 1.37; 95% CI 0.46-4.08, p = 0.57). There was no interaction between LGE and NSVT for the risk of all-cause mortality (p = 0.62). In patients with non-ischemic systolic HF there was no relationship between the presence of LGE and NSVT or any other Holter recorded ventricular tachyarrhythmia. LGE was associated with increased risk of mortality, independent of the presence of NSVT.

Non-sustained ventricular tachycardia (NSVT) is an independent predictor of sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM). This meta-analysis evaluates the prognostic value of late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) for predicting NSVT and its association with SCD in HCM. We screened electronic databases for studies evaluating the prognostic value of LGE in predicting NSVT and SCD in HCM patients. A random-effects model estimated pooled sensitivity, specificity, accuracy, predictive values, and likelihood ratios for NSVT prediction. Association between LGE extent and NSVT incidence was analyzed using weighted mean differences (WMDs), while pooled odds ratios (ORs) with 95% CIs were calculated to assess LGE's association with SCD. Among 20 studies, LGE showed a pooled sensitivity, specificity, and accuracy of 91.33% (95% CI: 88.81-93.86), 37.45% (95% CI: 31.60-43.31), and 52.86% (95% CI: 45.73-59.98), respectively, for NSVT prediction. Positive and negative likelihood ratios and predictive values were, 1.40 and 0.23, and 36.35% and 92.03%, respectively. Patients with NSVT had a significantly greater LGE extent than those without (WMD: 5.95%, 95% CI: 3.08-8.81, p < 0.0001). NSVT prevalence was 28.73% (95% CI: 20.91-36.54). Additionally, LGE presence and SCD were significantly associated (OR 3.64, 95% CI: 2.36-5.61, p < 0.00001). LGE on CMR shows high sensitivity but limited specificity and accuracy for NSVT prediction. Moreover, LGE presence was significantly associated with SCD, and NSVT patients had greater LGE extent. Nonetheless, variability in predictive values and likelihood ratios underscores the need to combine LGE with other imaging biomarkers. Question Can LGE on CMR predict NSVT and SCD in HCM patients? Findings LGE demonstrated high sensitivity but limited specificity for NSVT prediction. Moreover, LGE presence was significantly associated with SCD, and NSVT patients had greater LGE extent. Clinical relevance LGE on CMR is a valuable marker for NSVT prediction and SCD in HCM patients, but it is not widely integrated into clinical practice. Our study highlights the need to integrate LGE with other imaging biomarkers for improved risk stratification.

case presentation: A 48-year-old woman presents with exertional dyspnea and recurrent syncope. One year earlier, a permanent pacemaker was placed after she complained of fatigue and was found to have high-grade atrioventricular block. Now, she has echocardiographic evidence of moderate to severe left ventricular (LV) systolic dysfunction with regional wall-motion abnormalities. Nuclear imaging is notable for heterogeneous myocardial uptake of technetium Tc99m sestamibi, and coronary angiography reveals widely patent epicardial vessels. Multiple episodes of nonsustained ventricular tachycardia (VT) are documented on continuous ECG monitoring. What are the diagnostic considerations for this patient, and what further evaluations are indicated? This patient presents with dilated cardiomyopathy (DCM) with electric instability (DCM+E), which we define as conduction disease and arrhythmia out of proportion to the severity of LV systolic dysfunction. Diverse causes can result in DCM+E and fall into general categories of inflammatory, infectious, hereditary, and infiltrative processes. Cardiac presentation associated with these conditions is distinct from more common causes of DCM such as ischemic heart disease, viral myocarditis, valvular dysfunction, pregnancy, or substance abuse. Clinical features that are suggestive of DCM+E include supraventricular arrhythmias or conduction disease that precedes cardiomyopathy, multiple VT morphologies, and features suggestive of ischemic heart disease (Q waves, regional wall-motion abnormalities, perfusion defects, ventricular aneurysm) in the absence of epicardial stenoses. In this Clinician Update, we focus on the diagnostic approach to patients with DCM+E. Emphasis is placed on diagnoses that are relatively common or for which the clinical management would be impacted significantly by recognition of the underlying cause. Ischemic heart disease may present with conduction disease and a high burden of arrhythmia, especially in the setting of acute myocardial ischemia/infarction. The exclusion of obstructive coronary artery disease is strongly recommended in patients with DCM+E because atherosclerosis is so prevalent, evidence-based treatment is readily available, and the …

Incremental prognostic value of late gadolinium enhancement extent, transmurality, and pattern in patients with ischaemic cardiomyopathy

The prevalence and associated factors of myocardial involvement in Duchenne muscular dystrophy patients in the first decade of life.

Background: Late gadolinium enhancement (LGE) by cardiac MR (CMR) has been related to adverse clinical outcomes in patients with nonischemic dilated cardiomyopathy (NIDC). But, a statistically significant association between LGE and arrhythmic risk in NIDC has not been demonstrated consistently. This study evaluated the impact of the presence, location and pattern of LGE on arrhythmic risk prediction in NICM. Methods: This study included 365 patients (54±15years) with NICM who underwent CMR. The extent, location and pattern of LGE were categorized. We analyzed for the primary outcome of ventricular arrhythmia (VA) including sustained or nonsustained ventricular tachycardia (VT), appropriate implantable cardioverter-defibrillator (ICD) intervention and ventricular fibrillation (VF). Cardiac death and hospitalization for heart failure (HF) were evaluated as secondary outcomes. Results: LGE was seen in 267 (73 %) patients. During median follow-up of 44±36 months, patients with LGE had higher incidence of cardiac death (15 % vs. 2 %, p&lt;0.001), hospitalization for HF (40 % vs. 15 %, p&lt;0.001) and VA (14% vs. 6%, p=0.03). In multivariable analysis, the presence of LGE (HR 2.78; 95% CI 1.10-7.02; p=0.03) was the independent predictor of arrhythmias. Patients with extensive LGE had higher VA (32% vs. 10%, p&lt;0.001) with lower cumulative survival free of VA than those without extensive LGE (p=0.001). The frequent LGE location was as follows: LV septum 64%, LV-RV junction 42% and inferior 10%. VA was lower in patients with than without localized LGE limited to LV-RV junction (21% vs. 46%, p=0.005). Interestingly, while the incidence of ventricular arrhythmia was higher in patients with transmural LGE (29% vs. 10%, p=0.003), it was lower in those with patch LGE (2% vs. 16%, p=0.02) than the other patients. Conclusions: In patients with NICM, the LGE was an independent prognostic predictor of VA. Extensive LGE and specific location of LGE was related with the arrhythmic events.

Objective To explore the predictive value of routine echocardiographic and electrocardiographic parameters in late gadolinium enhancement (LGE) in hypertrophic cardiomyopathy (HCM). Methods The study population consisted of a consecutive series of 95 HCM patients.According to the presence of LGE on cardiac magnetic resonance (CMR), these patients were divided into two groups: HCM patients with LGE (n=71) and HCM patients without LGE (n=24). The parameters of routine echocardiography and electrocardiography were compared between the two groups. ROC and Logistic analysis were made to find the predictors of LGE. Results ①As compared to those without LGE, HCM patients with LGE had higher prevalence of chest pain (P=0.027), β-blocker treatment (P=0.024), increased maximal left ventricular wall thickness (MLVWT) (P<0.000 1), non-sustained ventricular tachycardia (P=0.034), prolonged the rate-corrected cardiac QT interval (QTc) (P=0.011), T-wave inversion (TWI) (P=0.009), but reduced early diastolic mitral annular velocity (e′) (P=0.001). ②Univariate predictors of LGE on CMR were: increased MLVWT, reduced e′, prolonged QTc and more TWI. Only MLVWT (OR=1.23, 95%CI=1.05-1.44, P=0.013) and e′(OR=1.23, 95%CI=0.52-0.96, P=0.028) remained independent after multivariable analysis. Furthermore, the ROC analysis showed that these two parameters had discriminative ability to identify those with LGE. To be specific, HCM patients with MLVWT≥21.5 mm or e′≤5.55 cm/s were more likely to present with LGE. ③The leads number of TWI was positively correlated with percentage of LGE in left ventricular mass (LGE%) (r=0.220, P=0.044), but there was no correlation between location of TWI on ECG and territory of LGE on CMR. Conclusions In HCM patients, MLVWT and e′ are independent predictors of LGE on CMR. Furthermore, although the leads number of TWI is correlated with LGE%, no correlation has been found between location of TWI on ECG and territory of LGE on CMR. Key words: Echocardiography; Cardiomyopathy, hypertrophic; Electrocardiography; Late gadolinium enhancement

Magnetic resonance imaging in the evaluation of idiopathic frequent premature ventricular complexes with normal ventricular function

Premature Ventricular Complexes and Nonsustained Ventricular Tachycardia in Cardiac Sarcoidosis.

Prognostic Value of Late Gadolinium Enhancement Detected on Cardiac Magnetic Resonance in Cardiac Sarcoidosis

P603Cardiac Magnetic Resonance evaluation and risk stratification of patients with unexplained or suspected arrhythmias

Improved Detection of Cardiac Sarcoidosis Using Magnetic Resonance with Myocardial T2 Mapping

Cardiovascular Imaging in Clinical Practice

An asymptomatic athletic 42-year-old man has an abnormal 12-lead ECG obtained during his initial employment examination at a new job (Figure 1). He had no family history of hypertrophic cardiomyopathy (HCM) or unexplained sudden deaths. Echocardiogram demonstrated a 13-mm ventricular septal thickness without systolic anterior motion of the mitral valve. The patient exercised on a standard Bruce protocol stress (exercise) echocardiogram for 12 minutes, without symptoms or arrhythmias, and with appropriate blood pressure augmentation. In the immediate recovery period, systolic anterior motion was absent and outflow tract velocities were normal. A 24-hour ambulatory (Holter) ECG demonstrated normal sinus rhythm without ventricular ectopy. This clinical evaluation left a number of unanswered questions for the patient regarding the diagnosis of HCM, prognosis, and whether a genetic heart disease was present in his family. Figure 1. Abnormal 12-lead ECG in a 42-year-old man demonstrating normal sinus rhythm with left anterior fascicular block, RSR′ in leads V1 and V2, and left ventricular hypertrophy. Since the early 1970s, cardiovascular imaging has played a critical role in describing the structure and function of the heart in HCM.1–5 Indeed, HCM is a disorder uniquely suited to noninvasive imaging, given HCM’s characteristic heterogeneous morphology and hemodynamics, including dynamic left ventricular (LV) outflow obstruction.2,3 For much of 40 years, echocardiography has been the dominant imaging technique, first with rudimentary M-mode and then ultimately 2-dimentional imaging and Doppler,2 now widely available and accessible. The past decade has witnessed the introduction of cardiac magnetic resonance (CMR) into clinical HCM practice.1,3–10 This contemporary technique provides images with high spatial and temporal resolution and sharp contrast between the myocardial border and blood pool, allowing precise measurements of LV wall thickness and complete tomographic reconstruction of the entire cardiac chamber (without …

The long-term outcome of athletes with frequent ventricular premature complexes (VPCs) and apparently normal heart has not been fully clarified. To evaluate the clinical and prognostic significance of VPCs and the influence of continuing sports activity during follow-up, we studied 120 healthy athletes (96 men; median age 16 years) in whom frequent VPCs (>100 VPCs/24 hours) were discovered by chance during preparticipation screening. All athletes were followed up for a median of 84 months. During follow-up, 96 underwent serial 24-hour Holter recording and 62 underwent serial echocardiography. The median number of VPCs/24 hours on basal Holter was 3,760. During follow-up, 81 athletes continued sports activity, whereas 39 did not. No athlete died or developed overt heart disease. The median number of VPCs/24 hours decreased in both athletes who continued sports activity and those who did not (from 3,805 to 1,124, p <0.0001 and from 5,787 to 1,298, p <0.0001, respectively). During follow-up, left ventricular ejection fraction slightly decreased to <55% in 9 of 62 athletes who, in respect to the remaining 53, had more VPCs/24 hours both in the basal state (12,000 vs 3,880) and during follow-up (10,702 vs 1,368), and a longer follow-up (95 vs 36 months). In conclusion, (1) frequent VPCs in athletes without heart disease have a long-term benign prognostic significance, (2) sporting activity does not modify this benign outcome, (3) during follow-up, the burden of VPCs decreases whether or not subjects continue sports activity, and (4) in 14.5% of athletes, ejection fraction slightly decreases over time.