Cardiovascular magnetic resonance predictors of heart failure in hypertrophic cardiomyopathy: the role of myocardial replacement fibrosis and the microcirculation.

INTRODUCTION: Heart failure (HF) in hypertrophic cardiomyopathy (HCM) is associated with high morbidity and mortality. Predictors of HF, in particular the role of myocardial fibrosis and microvascular ischemia remain unclear. We assessed the predictive value of cardiovascular magnetic resonance (CMR) for development of HF in HCM in an observational cohort study. METHODS: Serial patients with HCM underwent CMR, including adenosine first-pass perfusion, left atrial (LA) and left ventricular (LV) volumes indexed to body surface area (i) and late gadolinium enhancement (%LGE- as a % of total myocardial mass). We used a composite endpoint of HF death, cardiac transplantation, and progression to NYHA class III/IV. RESULTS: A total of 543 patients with HCM underwent CMR, of whom 94 met the composite endpoint at baseline. The remaining 449 patients were followed for a median of 5.6 years. Thirty nine patients (8.7%) reached the composite endpoint of HF death (n = 7), cardiac transplantation (n = 2) and progression to NYHA class III/IV (n = 20). The annual incidence of HF was 2.0 per 100 person-years, 95% CI (1.6-2.6). Age, previous non-sustained ventricular tachycardia, LV end-systolic volume indexed to body surface area (LVESVI), LA volume index ; LV ejection fraction, %LGE and presence of mitral regurgitation were significant univariable predictors of HF, with LVESVI (Hazard ratio (HR) 1.44, 95% confidence interval (95% CI) 1.16-1.78, p = 0.001), %LGE per 10% (HR 1.44, 95%CI 1.14-1.82, p = 0.002) age (HR 1.37, 95% CI 1.06-1.77, p = 0.02) and mitral regurgitation (HR 2.6, p = 0.02) remaining independently predictive on multivariable analysis. The presence or extent of inducible perfusion defect assessed using a visual score did not predict outcome (p = 0.16, p = 0.27 respectively). DISCUSSION: The annual incidence of HF in a contemporary ambulatory HCM population undergoing CMR is low. Myocardial fibrosis and LVESVI are strongly predictive of future HF, however CMR visual assessment of myocardial perfusion was not.

Recognition and significance of pathological T-wave inversions in athletes.

BACKGROUND: Pathological T-wave inversion (PTWI) is rarely observed on the ECG of healthy athletes, whereas it is common in patients with certain cardiac diseases. All ECG interpretation guidelines for use within athletes state that PTWI (except in leads aVR, III and V1 and in V1-V4 when preceded by domed ST segment in asymptomatic Afro-Caribbean athletes only) cannot be considered a physiological adaptation. The aims of the present study were to prospectively determine the prevalence of cardiac pathology in athletes presenting with PTWI, and to examine the efficacy of cardiac magnetic resonance in the work-up battery of further examinations. METHODS AND RESULTS: Athletes presenting with PTWI (n=155) were investigated with clinical examination, ECG, echocardiography, exercise testing, 24h Holter ECG, and cardiac magnetic resonance. Cardiac disease was established in 44.5% of athletes, with hypertrophic cardiomyopathy (81%) the most common pathology. Echocardiography was abnormal in 53.6% of positive cases, and cardiac magnetic resonance identified a further 24 athletes with disease. Five athletes (7.2%) considered normal on initial presentation subsequently expressed pathology during follow-up. Familial history of sudden cardiac death and ST-segment depression associated with PTWI were predictive of cardiac disease. CONCLUSIONS: PTWI should be considered pathological in all cases until proven otherwise, because it was associated with cardiac pathology in 45% of athletes. Despite echocardiography identifying pathology in half of these cases, cardiac magnetic resonance must be considered routine in athletes presenting with PTWI with normal echocardiography. Although exclusion from competitive sport is not warranted in the presence of normal secondary examinations, annual follow-up is essential to ascertain possible disease expression.

LV Apical Rupture Complicating Acute Myocardial Infarction: The Role of CMR.

PURPOSE: This case illustrates an acute myocardial infarction with occlusion of the left anterior descending coronary artery complicated by apical ventricular rupture and apical thrombus. PROCEDURES: An electrocardiogram, transthoracic echocardiogram (TTE), coronary angiography and cardiac magnetic resonance imaging (CMR) guided optimal management of the patient. FINDINGS: Coronary angiography revealed multivessel disease with an ostial occlusion of the LAD. Echocardiography showed apical dilatation of the left ventricle with a large, echogenic mass at the apex. Contrast echocardiography confirmed the presence of a large apical thrombus, separated from the LV cavity by myocardium. A CMR showed a completed LAD infarct and a filling thrombus was noted in the aneurysmal apical region inferring a contained rupture of the LV apex. PRINCIPLE CONCLUSIONS: Accurate and definitive delineation of unusual cardiac anatomy is best provided by complementary multimodality cardiac imaging, echocardiography and CMR. TTE can miss LV thrombi, particularly when they are large, aneurysmal and apical in nature. CMR provides the cardiac surgeon the ability to visualise in 3D the functional and morphological abnormalities, helping guide necessary intervention. Optimal management of patients with ventricular rupture remains controversial both in terms of timing and choice of intervention.

Coronary microvascular ischemia in hypertrophic cardiomyopathy - a pixel-wise quantitative cardiovascular magnetic resonance perfusion study.

BACKGROUND: Microvascular dysfunction in HCM has been associated with adverse clinical outcomes. Advances in quantitative cardiovascular magnetic resonance (CMR) perfusion imaging now allow myocardial blood flow to be quantified at the pixel level. We applied these techniques to investigate the spectrum of microvascular dysfunction in hypertrophic cardiomyopathy (HCM) and to explore its relationship with fibrosis and wall thickness. METHODS: CMR perfusion imaging was undertaken during adenosine-induced hyperemia and again at rest in 35 patients together with late gadolinium enhancement (LGE) imaging. Myocardial blood flow (MBF) was quantified on a pixel-by-pixel basis from CMR perfusion images using a Fermi-constrained deconvolution algorithm. Regions-of-interest (ROI) in hypoperfused and hyperemic myocardium were identified from the MBF pixel maps. The myocardium was also divided into 16 AHA segments. RESULTS: Resting MBF was significantly higher in the endocardium than in the epicardium (mean ± SD: 1.25 ± 0.35 ml/g/min versus 1.20 ± 0.35 ml/g/min, P<0.001), a pattern that reversed with stress (2.00 ± 0.76 ml/g/min versus 2.36 ± 0.83 ml/g/min, P<0.001). ROI analysis revealed 11 (31%) patients with stress MBF lower than resting values (1.05 ± 0.39 ml/g/min versus 1.22 ± 0.36 ml/g/min, P=0.021). There was a significant negative association between hyperemic MBF and wall thickness (ß=-0.047 ml/g/min per mm, 95% CI: -0.057 to -0.038, P<0.001) and a significantly lower probability of fibrosis in a segment with increasing hyperemic MBF (odds ratio per ml/g/min: 0.086, 95% CI: 0.078 to 0.095, P=0.003). CONCLUSIONS: Pixel-wise quantitative CMR perfusion imaging identifies a subgroup of patients with HCM that have localised severe microvascular dysfunction which may give rise to myocardial ischemia.

Long-term clinical outcomes after unprotected left main coronary artery stenting in an all-comers patient population.

BACKGROUND: The goal of treating patients with coronary artery disease is to improve survival and relieve symptoms. Several studies have compared the safety and efficacy of left main coronary artery (LMCA) stenting and coronary-artery bypass grafting in case control and randomized trials. OBJECTIVE: In this study we present the long term outcome of stenting unprotected LMCA stenosis in day to day practice in unselected patients. METHODS: One hundred and fifty eight patients were prospectively recruited with symptomatic unprotected LMCA stenosis undergoing percutaneous coronary intervention (PCI). Using the euroSCORE, each patient's surgical mortality risk was estimated. Study end-points were any major adverse cardiac event (MACE) defined as cardiac death, nonfatal myocardial infarction, or target lesion revascularization at follow-up with either CABG or repeat PCI. RESULTS: The mean follow-up was 54 ± 25 months. The mean euroSCORE was 10.6 ± 13.4 (0.9-71) and the mean SYNTAX score was 39.6 ± 10.7 (10-65). The MACE rate was 11.4% at a mean follow up of 54 months. Six (3.8%) patients suffered postprocedure myocardial infarction. There were 24 (15%) deaths of which 12 were cardiac (mean euroSCORE 21.6 ± 5.5 P < 0.001). Repeat angiography was performed in 88 (55.7%) patients. Seven (4.4%) patients had in-stent restenosis; three occurred in BMS (P = 0.06). Two patients underwent revascularization with CABG and five had successful repeat PCI. CONCLUSION: In this on-going registry of high risk patients with LMCA stenosis, stenting was found to be safe and clinically effective in maintaining event-free survival.

Natriuretic peptide-based screening and collaborative care for heart failure: the STOP-HF randomized trial.

IMPORTANCE: Prevention strategies for heart failure are needed. OBJECTIVE: To determine the efficacy of a screening program using brain-type natriuretic peptide (BNP) and collaborative care in an at-risk population in reducing newly diagnosed heart failure and prevalence of significant left ventricular (LV) systolic and/or diastolic dysfunction. DESIGN, SETTING, AND PARTICIPANTS: The St Vincent's Screening to Prevent Heart Failure Study, a parallel-group randomized trial involving 1374 participants with cardiovascular risk factors (mean age, 64.8 [SD, 10.2] years) recruited from 39 primary care practices in Ireland between January 2005 and December 2009 and followed up until December 2011 (mean follow-up, 4.2 [SD, 1.2] years). INTERVENTION: Patients were randomly assigned to receive usual primary care (control condition; n=677) or screening with BNP testing (n=697). Intervention-group participants with BNP levels of 50 pg/mL or higher underwent echocardiography and collaborative care between their primary care physician and specialist cardiovascular service. MAIN OUTCOMES AND MEASURES: The primary end point was prevalence of asymptomatic LV dysfunction with or without newly diagnosed heart failure. Secondary end points included emergency hospitalization for arrhythmia, transient ischemic attack, stroke, myocardial infarction, peripheral or pulmonary thrombosis/embolus, or heart failure. RESULTS: A total of 263 patients (41.6%) in the intervention group had at least 1 BNP reading of 50 pg/mL or higher. The intervention group underwent more cardiovascular investigations (control, 496 per 1000 patient-years vs intervention, 850 per 1000 patient-years; incidence rate ratio, 1.71; 95% CI, 1.61-1.83; P<.001) and received more renin-angiotensin-aldosterone system-based therapy at follow-up (control, 49.6%; intervention, 56.5%; P=.01). The primary end point of LV dysfunction with or without heart failure was met in 59 (8.7%) of 677 in the control group and 37 (5.3%) of 697 in the intervention group (odds ratio [OR], 0.55; 95% CI, 0.37-0.82; P = .003). Asymptomatic LV dysfunction was found in 45 (6.6%) of 677 control-group patients and 30 (4.3%) of 697 intervention-group patients (OR, 0.57; 95% CI, 0.37-0.88; P = .01). Heart failure occurred in 14 (2.1%) of 677 control-group patients and 7 (1.0%) of 697 intervention-group patients (OR, 0.48; 95% CI, 0.20-1.20; P = .12). The incidence rates of emergency hospitalization for major cardiovascular events were 40.4 per 1000 patient-years in the control group vs 22.3 per 1000 patient-years in the intervention group (incidence rate ratio, 0.60; 95% CI, 0.45-0.81; P = .002). CONCLUSION AND RELEVANCE: Among patients at risk of heart failure, BNP-based screening and collaborative care reduced the combined rates of LV systolic dysfunction, diastolic dysfunction, and heart failure. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00921960.

Association of fibrosis with mortality and sudden cardiac death in patients with nonischemic dilated cardiomyopathy.

IMPORTANCE: Risk stratification of patients with nonischemic dilated cardiomyopathy is primarily based on left ventricular ejection fraction (LVEF). Superior prognostic factors may improve patient selection for implantable cardioverter-defibrillators (ICDs) and other management decisions. OBJECTIVE: To determine whether myocardial fibrosis (detected by late gadolinium enhancement cardiovascular magnetic resonance [LGE-CMR] imaging) is an independent and incremental predictor of mortality and sudden cardiac death (SCD) in dilated cardiomyopathy. DESIGN, SETTING, AND PATIENTS: Prospective, longitudinal study of 472 patients with dilated cardiomyopathy referred to a UK center for CMR imaging between November 2000 and December 2008 after presence and extent of midwall replacement fibrosis were determined. Patients were followed up through December 2011. MAIN OUTCOME MEASURES: Primary end point was all-cause mortality. Secondary end points included cardiovascular mortality or cardiac transplantation; an arrhythmic composite of SCD or aborted SCD (appropriate ICD shock, nonfatal ventricular fibrillation, or sustained ventricular tachycardia); and a composite of HF death, HF hospitalization, or cardiac transplantation. RESULTS: Among the 142 patients with midwall fibrosis, there were 38 deaths (26.8%) vs 35 deaths (10.6%) among the 330 patients without fibrosis (hazard ratio [HR], 2.96 [95% CI, 1.87-4.69]; absolute risk difference, 16.2% [95% CI, 8.2%-24.2%]; P < .001) during a median follow-up of 5.3 years (2557 patient-years of follow-up). The arrhythmic composite was reached by 42 patients with fibrosis (29.6%) and 23 patients without fibrosis (7.0%) (HR, 5.24 [95% CI, 3.15-8.72]; absolute risk difference, 22.6% [95% CI, 14.6%-30.6%]; P < .001). After adjustment for LVEF and other conventional prognostic factors, both the presence of fibrosis (HR, 2.43 [95% CI, 1.50-3.92]; P < .001) and the extent (HR, 1.11 [95% CI, 1.06-1.16]; P < .001) were independently and incrementally associated with all-cause mortality. Fibrosis was also independently associated with cardiovascular mortality or cardiac transplantation (by fibrosis presence: HR, 3.22 [95% CI, 1.95-5.31], P < .001; and by fibrosis extent: HR, 1.15 [95% CI, 1.10-1.20], P < .001), SCD or aborted SCD (by fibrosis presence: HR, 4.61 [95% CI, 2.75-7.74], P < .001; and by fibrosis extent: HR, 1.10 [95% CI, 1.05-1.16], P < .001), and the HF composite (by fibrosis presence: HR, 1.62 [95% CI, 1.00-2.61], P = .049; and by fibrosis extent: HR, 1.08 [95% CI, 1.04-1.13], P < .001). Addition of fibrosis to LVEF significantly improved risk reclassification for all-cause mortality and the SCD composite (net reclassification improvement: 0.26 [95% CI, 0.11-0.41]; P = .001 and 0.29 [95% CI, 0.11-0.48]; P = .002, respectively). CONCLUSIONS AND RELEVANCE: Assessment of midwall fibrosis with LGE-CMR imaging provided independent prognostic information beyond LVEF in patients with nonischemic dilated cardiomyopathy. The role of LGE-CMR in the risk stratification of dilated cardiomyopathy requires further investigation.

Diagnostic and prognostic value of cardiovascular magnetic resonance in non-ischaemic cardiomyopathies.

Cardiovascular Magnetic Resonance (CMR) is recognised as a valuable clinical tool which in a single scan setting can assess ventricular volumes and function, myocardial fibrosis, iron loading, flow quantification, tissue characterisation and myocardial perfusion imaging. The advent of CMR using extrinsic and intrinsic contrast-enhanced protocols for tissue characterisation have dramatically changed the non-invasive work-up of patients with suspected or known cardiomyopathy. Although the technique initially focused on the in vivo identification of myocardial necrosis through the late gadolinium enhancement (LGE) technique, recent work highlighted the ability of CMR to provide more detailed in vivo tissue characterisation to help establish a differential diagnosis of the underlying aetiology, to exclude an ischaemic substrate and to provide important prognostic markers. The potential application of CMR in the clinical approach of a patient with suspected non-ischaemic cardiomyopathy is discussed in this review.

Imaging focal and interstitial fibrosis with cardiovascular magnetic resonance in athletes with left ventricular hypertrophy: implications for sporting participation.

Long-term high-intensity physical activity is associated with morphological changes, termed as the 'athlete's heart'. The differentiation of physiological cardiac adaptive changes in response to high-level exercise from pathological changes consistent with an inherited cardiomyopathy is imperative. Cardiovascular magnetic resonance (CMR) imaging allows definition of abnormal processes occurring at the tissue level, including, importantly, myocardial fibrosis. It is therefore vital in accurately making this differentiation. In this review, we will review the role of CMR imaging of fibrosis, and detail CMR characterisation of myocardial fibrosis in various cardiomyopathies, and the implications of fibrosis. Additionally, we will outline advances in imaging fibrosis, in particular T1 mapping. Finally we will address the role of CMR in pre-participation screening.

Do big athletes have big hearts? Impact of extreme anthropometry upon cardiac hypertrophy in professional male athletes.

AIM: Differentiating physiological cardiac hypertrophy from pathology is challenging when the athlete presents with extreme anthropometry. While upper normal limits exist for maximal left ventricular (LV) wall thickness (14 mm) and LV internal diameter in diastole (LVIDd, 65 mm), it is unknown if these limits are applicable to athletes with a body surface area (BSA) >2.3 m(2). PURPOSE: To investigate cardiac structure in professional male athletes with a BSA>2.3 m(2), and to assess the validity of established upper normal limits for physiological cardiac hypertrophy. METHODS: 836 asymptomatic athletes without a family history of sudden death underwent ECG and echocardiographic screening. Athletes were grouped according to BSA (Group 1, BSA>2.3 m(2), n=100; Group 2, 2-2.29 m(2), n=244; Group 3, <1.99 m(2), n=492). RESULTS: There was strong linear relationship between BSA and LV dimensions; yet no athlete with a normal ECG presented a maximal wall thickness and LVIDd greater than 13 and 65 mm, respectively. In Group 3 athletes, Black African ethnicity was associated with larger cardiac dimensions than either Caucasian or West Asian ethnicity. Three athletes were diagnosed with a cardiomyopathy (0.4% prevalence); with two athletes presenting a maximal wall thickness >13 mm, but in combination with an abnormal ECG suspicious of an inherited cardiac disease. CONCLUSION: Regardless of extreme anthropometry, established upper limits for physiological cardiac hypertrophy of 14 mm for maximal wall thickness and 65 mm for LVIDd are clinically appropriate for all athletes. However, the abnormal ECG is key to diagnosis and guides follow-up, particularly when cardiac dimensions are within accepted limits.

Hypertrophic cardiomyopathy and ultra-endurance running - two incompatible entities?

Regular and prolonged exercise is associated with increased left ventricular wall thickness that can overlap with hypertrophic cardiomyopathy (HCM). Differentiating physiological from pathological hypertrophy has important implications, since HCM is the commonest cause of exercise-related sudden cardiac death in young individuals. Most deaths have been reported in intermittent 'start-stop' sports such as football (soccer) and basketball. The theory is that individuals with HCM are unable to augment stroke volume sufficiently to meet the demands of endurance sports and are accordingly 'selected-out' of participation in such events. We report the case of an ultra-endurance athlete with 25 years of > 50 km competitive running experience, with genetically confirmed HCM; thereby demonstrating that these can be two compatible entities.

The prehospital patient pathway and experience of care with acute heart failure: a comparison of two health care systems.

AIMS: This study aimed to analyse community management of patients during the symptomatic period prior to admission with acute decompensated heart failure (ADHF). METHODS AND RESULTS: We conducted a prospective, two-centre, two-country observational study evaluating care pathways and patient experience in patients admitted to hospital with ADHF. Quantitative and qualitative data were gathered from patients, carers, and general practitioners (GPs). From the Irish centre, 114 patients enrolled, and from the English centre, 50 patients. Symptom duration longer than 72 h prior to hospitalization was noted among 70.4% (76) Irish and 80% (40) English patients, with no significant difference between those with a new diagnosis of HF [de novo HF (dnHF)] and those with known HF [established HF (eHF)] in either cohort. For the majority, dyspnoea was the dominant symptom; however, 63.3% (31) of these Irish patients and 47.2% (17) of these English patients did not recognize this as an HF symptom, with no significant difference between dnHF and eHF patients. Of the 46.5% (53) of Irish and 38% (19) of English patients reviewed exclusively by GPs before hospitalization, numbers prescribed diuretics were low (11.3%, six; and 15.8%, three, respectively); eHF patients were no more likely to receive diuretics than dnHF patients. Barriers to care highlighted by GPs included inadequate access to basic diagnostics, specialist support and up-to-date patient information, and lack of GP comfort in managing HF. CONCLUSION: The aforementioned findings, consistent across both health care jurisdictions, show a clear potential to intervene earlier and more effectively in ADHF or to prevent the need for hospitalization.

Troponin release following endurance exercise: is inflammation the cause? a cardiovascular magnetic resonance study.

BACKGROUND: The aetiology and clinical significance of troponin release following endurance exercise is unclear but may be due to transient myocardial inflammation. Cardiovascular magnetic resonance (CMR) affords us the opportunity to evaluate the presence of myocardial inflammation and focal fibrosis and is the ideal imaging modality to study this hypothesis. We sought to correlate the relationship between acute bouts of ultra endurance exercise leading to cardiac biomarkers elevation and the presence of myocardial inflammation and fibrosis using CMR. METHODS: 17 recreation athletes (33.5 +/- 6.5 years) were studied before and after a marathon run with troponin, NTproBNP, and CMR. Specific imaging parameters to look for inflammation included T2 weighted images, and T1 weighted spin-echo images before and after an intravenous gadolinium-DTPA to detect myocardial hyperemia secondary to inflammation. Late gadolinium imaging was performed (LGE) to detect any focal regions of replacement fibrosis. RESULTS: Eleven of the 17 participant had elevations of TnI above levels of cut off for myocardial infarction 6 hrs after the marathon (0.075 +/- 0.02, p = 0.007). Left ventricular volumes were reduced post marathon and a small increase in ejection fraction was noted (64+/- 1% pre, 67+/- 1.2% post, P = 0.014). Right ventricular volumes, stroke volume, and ejection fraction were unchanged post marathon. No athlete fulfilled criteria for myocardial inflammation based on current criteria. No regions of focal fibrosis were seen in any of the participants. CONCLUSION: Exercise induced cardiac biomarker release is not associated with any functional changes by CMR or any detectable myocardial inflammation or fibrosis.

Predictors and Mechanisms of Atrial Fibrillation in Patients With Hypertrophic Cardiomyopathy.

Atrial fibrillation (AF) in hypertrophic cardiomyopathy (HC) is associated with significant symptomatic deterioration, heart failure, and thromboembolic disease. There is a need for better mechanistic insight and improved identification of at risk patients. We used cardiovascular magnetic resonance (CMR) to assess predictors of AF in HC, in particular the role of myocardial fibrosis. Consecutive patients with HC referred for CMR 2003 to 2013 were prospectively enrolled. CMR parameters including left ventricular volumes, presence and percentage of late gadolinium enhancement in the left ventricle (%LGE) and left atrial volume index (LAVi) were measured. Overall, 377 patients were recruited (age 62 ± 14 years, 73% men). Sixty-two patients (16%) developed new-onset AF during a median follow up of 4.5 (interquartile range 2.9 to 6.0) years. Multivariable analysis revealed %LGE (hazard ratio [HR] 1.3 per 10% (confidence interval: 1.0 to 1.5; p = 0.02), LAVi (HR 1.4 per 10 mL/m2[1.2 to 1.5; p < 0.001]), age at HC diagnosis, nonsustained ventricular tachycardia and diabetes to be independent predictors of AF. We constructed a simple risk prediction score for future AF based on the multivariable model with a Harrell's C-statistic of 0.73. In conclusion, the extent of ventricular fibrosis and LA volume independently predicted AF in patients with HC. This finding suggests a mechanistic relation between fibrosis and future AF in HC. CMR with quantification of fibrosis has incremental value over LV and LA measurements in risk stratification for AF. A risk prediction score may be used to identify patients at high risk of future AF who may benefit from more intensive rhythm monitoring and a lower threshold for oral anticoagulation.

Cardiovascular magnetic resonance of cardiomyopathies.

Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with architectural abnormalities and mechanical dysfunction. Recent advances in our understanding of the genetics, pathophysiology, and natural history of these conditions has resulted in better diagnosis and management, leading to improvements in mortality. Major developments in imaging techniques, in particular contrast-enhanced MRI, now permit in vivo tissue characterization of the myocardium. Through defining disease severity, etiology, and to some extent in risk stratification, routine cardiovascular magnetic resonance evaluation of this group of patients provides essential information required in everyday clinical practice.

Cardiovascular magnetic resonance in the evaluation of hypertrophic and infiltrative cardiomyopathies.

There is often considerable phenotypic overlap in hypertrophic and infiltrative cardiomyopathies. This overlap creates difficulties, when using routine imaging modalities, in arriving at a conclusive diagnosis. Cardiovascular magnetic resonance (CMR) can make diagnosis easier and more certain. Used with gadolinium contrast agent for tissue characterization, CMR offers a superior field of view and temporal resolution, enabling clinicians to make more confident assessments of etiology. CMR may also be a useful modality for stratifying risk and monitoring treatment responses over time in patients with hypertrophic or infiltrative cardiomyopathies. This article highlights the role of CMR in the assessment and, if relevant, the risk stratification of hypertrophic and infiltrative cardiomyopathies.

The biologic variability of B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide in stable heart failure patients.

BACKGROUND: There are conflicting data on the usefulness of B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) in the optimization of therapy for heart failure (HF). Discordant results may be explained by the intra-individual variability of these peptides. This study evaluates the intraindividual variability of BNP and NT-proBNP and the impact of the covariates of age, sex, and renal function. METHODS AND RESULTS: Stable HF patients attending our unit were included. Blood samples were drawn 1 hour apart on 2 occasions 1 week apart. Forty-five patients were enrolled (69.6 +/- 12.1 years, 64% male, 84% systolic HF). Within-hour and within-week intraindividual variability were: 6.9% and 21.1% for NT-proBNP; 14.6% and 28.4% for BNP (P < .01 for within-hour comparison of BNP and NT-proBNP). Reference change values over 1 week for NT-proBNP and BNP were 49.2% and 66.2%, respectively. There were no significant relationships identified between variability and age, gender, or glomerular filtration rate. CONCLUSION: There is considerable intraindividual variability in these peptides in stable HF patients. Changes of approximately 50% and 66% for NT-proBNP and BNP from week to week are needed to indicate an altered clinical status and caution should be exercised in interpreting serial changes in these peptide levels when monitoring patient responses to treatment or clinical status.

Severely impaired left ventricular function: tissue characterization by cardiovascular magnetic resonance in a clinical dilemma.

In patients with symptoms of heart failure, identifying the underlying cause of cardiomyopathy is helpful to establish the diagnosis and to guide therapy. The differential diagnosis of cardiomyopathy can be challenging based on clinical findings. We report the case of a patient who represented a clinical dilemma (cardiac sarcoidosis or ischaemic heart disease), in whom cardiovascular magnetic resonance was a clinically valuable tool to distinguish dual cardiac pathology due to its unique, non-invasive, tissue characterization capabilities.