Absence Of Left Ventricular Dysfunction Research Articles

Routine beta-blocker therapy after acute coronary syndromes: The end of an era?

Beta-blocker therapy, a treatment burdened by side effects including fatigue, erectile dysfunction and depression, was shown to reduce mortality and cardiovascular events after acute coronary syndromes (ACS) in the pre-coronary reperfusion era. Potential mechanisms include protection from ventricular arrhythmias, increased ischaemia threshold and prevention of left ventricular (LV) adverse remodelling. With the advent of early mechanical reperfusion and contemporary pharmacologic secondary prevention, the benefit of beta-blockers after ACS in the absence of LV dysfunction has been challenged. The present narrative review discusses the contemporary evidence based on searching the PubMed database and references in identified articles. Recently, the REDUCE-AMI trial-the first adequately powered randomized trial in the reperfusion era to test beta-blocker therapy after myocardial infarction with preserved left ventricular ejection fraction (LVEF)-showed no benefit on the composite of all-cause death or myocardial infarction over a median 3.5-year follow-up. While the benefit of beta-blockers in patients with reduced LVEF remains undisputed, their value in post-ACS patients with mildly reduced systolic function (LVEF 41%-49%) has not been studied in contemporary randomized trials; in this setting, observational studies have suggested a reduction in cardiovascular events with these agents. The adequate duration of beta-blocker therapy remains unknown, but observational data suggests that any mortality benefit may be lost beyond 1-12 months after ACS in patients with LVEF >40%. We believe that there is sufficient evidence to abandon routine beta-blocker prescription in post-ACS patients with preserved LV systolic function.

Atrial mitral regurgitation: Characteristics and outcomes of transcatheter mitral valve edge‐to‐edge repair

Mitral transcatheter edge-to-edge repair (MTEER) is an established therapeutic approach for mitral regurgitation (MR). Functional mitral regurgitation originating from atrial myopathy (A-FMR) has been described. We sought to assess the clinical, echocardiographic and hemodynamic considerations in A-FMR patients undergoing MTEER. From 2014 to 2020, patients undergoing MTEER for degenerative MR (DMR), functional MR (FMR), and mixed MR were assessed. A-FMR was defined by the presence of MR > moderate in severity; left ventricular (LV) ejection fraction (LVEF) ≥ 50%; and severe left atrial (LA) enlargement in the absence of LV dysfunction, leaflet pathology, or LV tethering. The diagnosis of A-FMR (vs. ventricular-FMR [V-FMR]) was confirmed by three independent echocardiographers. Baseline characteristics, procedural outcomes as well as clinical and echocardiographic follow-up are reported. Device success was defined as final MR grade ≤ moderate; MR reduction ≥1 grade; and final transmitral gradient <5 mmHg. 306 patients underwent MTEER, including DMR (62%), FMR (19%), and mixed MR (19%). FMR cases included 37 (63.8%) V-FMR and 21 (36.2%) A-FMR. Tricuspid regurgitation (≥ moderate) was higher in A-FMR (80.1%) compared to V-FMR (54%) and DMR (42%). Device success did not significantly differ between A-FMR and V-FMR (57% vs. 73%, p = 0.34) or DMR (57% vs. 64%, p = 1.0). The A-FMR cohort was less likely to achieve ≥3 grades of MR reduction compared to V-FMR (19% vs. 54%, p = 0.01) and DMR (19% vs. 49.7%, p = 0.01). Patients with V-FMR and DMR demonstrated significant reductions in mean left atrial pressure (LAP) and peak LA V-wave, though A-FMR did not (LAP -0.24 ± 4.9, p = 0.83; peak V-wave -1.76 ± 9.1, p = 0.39). In follow-up, echocardiographic and clinical outcomes were similar. In patients undergoing MTEER, A-FMR represents one-third of FMR cases. A-FMR demonstrates similar procedural success but blunted acute hemodynamic responses compared with DMR and V-FMR following MTEER. Dedicated studies specifically considering A-FMR are needed to discern the optimal therapeutic approaches.

Outcome and durability of mitral valve annuloplasty in atrial secondary mitral regurgitation

ObjectivesAtrial secondary mitral regurgitation (ASMR) is a clinically distinct form of Carpentier type I mitral regurgitation (MR), rooted in excessive atrial and mitral annular dilation in the absence of left...

Delayed onset Takotsubo syndrome following exercise ECG: a case report.

BackgroundTakotsubo syndrome usually occurs immediately following a physical or emotional trigger. In some cases, a triggering stress may not be evident. A delayed manifestation of the syndrome may account for such cases.Case summaryAn asymptomatic 69-year-old woman presented for a routine cardiac check-up, which revealed normal electrocardiogram (ECG), echocardiography, and exercise ECG. She did not complain of any chest pain during or immediately after the tests. After about 24 h, she developed chest pain for which she was admitted with the provisional diagnosis of acute coronary syndrome. ECG showed dynamic T-wave changes with QTc prolongation. Cardiac biomarkers were mildly elevated. Characteristic reversible left ventricular dysfunction in absence of coronary stenosis ultimately led to the diagnosis of Takotsubo syndrome.DiscussionOur case represents a delayed occurrence of Takotsubo syndrome triggered by a treadmill exercise stress test, which manifested about 24 h following the stressor. Such delayed manifestation may account for those cases of Takotsubo syndrome where no immediate triggering stressor is evident.

Adult onset still’s disease masquerading as acute coronary syndrome

Adult onset still’s disease (AOSD) is a rare inflammatory disorder characterized by high fevers, arthralgia, salmon rash and leukocytosis. It is a diagnosis of exclusion and popularly diagnosed by the Yamaguchi criteria. Cardiac involvement in AOSD causing myocarditis is seldom seen. Echocardiography is an important measure of cardiac manifestation, but a more characteristic confirmation is obtained by the cardiac MRI. It is an increasingly recognized noninvasive alternative to the gold standard endomyocardial biopsy. In this case, mid myocardial enhancement in the absence of left ventricular dysfunction was consistent with a diagnosis of myocarditis in AOSD. The delay in diagnosis was caused by AOSD masquerading as acute coronary syndrome. This case highlights the importance of early recognition of myocarditis in an atypical presentation of AOSD which results in early immunomodulatory therapy and an improved clinical outcome.

Increased Echogenicity and Radiodense Foci on Echocardiogram and MicroCT in Murine Myocarditis.

ObjectivesTo address the question as to whether echocardiographic and/or microcomputed tomography (microCT) analysis can be utilized to assess the extent of Coxsackie B virus (CVB) induced myocarditis in the absence of left ventricular dysfunction in the mouse.BackgroundViral myocarditis is a significant clinical problem with associated inflammation of the myocardium and myocardial injury. Murine models of myocarditis are commonly used to study the pathophysiology of the disease, but methods for imaging the mouse myocardium have been limited to echocardiographic assessment of ventricular dysfunction and, to a lesser extent, MRI imaging.MethodsUsing a murine model of myocarditis, we used both echocardiography and microCT to assess the extent of myocardial involvement in murine myocarditis using both wild-type mice and CVB cleavage-resistant dystrophin knock-in mice.ResultsAreas of increased echogenicity were only observed in the myocardium of Coxsackie B virus infected mice. These echocardiographic abnormalities correlated with the extent of von Kossa staining (a marker of membrane permeability), inflammation, and fibrosis. Given that calcium phosphate uptake as imaged by von Kossa staining might also be visualized using microCT, we utilized microCT imaging which allowed for high-resolution, 3-dimensional images of radiodensities that likely represent calcium phosphate uptake. As with echocardiography, only mice infected with Coxsackie B virus displayed abnormal accumulation of calcium within individual myocytes indicating increased membrane permeability only upon exposure to virus.ConclusionsThese studies demonstrate new, quantitative, and semi-quantitative imaging approaches for the assessment of myocardial involvement in the setting of viral myocarditis in the commonly utilized mouse model of viral myocarditis.

Baroreflex failure increases the risk of pulmonary edema in conscious rats with normal left ventricular function.

In heart failure with preserved ejection fraction (HFpEF), the complex pathogenesis hinders development of effective therapies. Since HFpEF and arteriosclerosis share common risk factors, it is conceivable that stiffened arterial wall in HFpEF impairs baroreflex function. Previous investigations have indicated that the baroreflex regulates intravascular stressed volume and arterial resistance in addition to cardiac contractility and heart rate. We hypothesized that baroreflex dysfunction impairs regulation of left atrial pressure (LAP) and increases the risk of pulmonary edema in freely moving rats. In 15-wk Sprague-Dawley male rats, we conducted sinoaortic denervation (SAD, n = 6) or sham surgery (Sham, n = 9), and telemetrically monitored ambulatory arterial pressure (AP) and LAP. We compared the mean and SD (lability) of AP and LAP between SAD and Sham under normal-salt diet (NS) or high-salt diet (HS). SAD did not increase mean AP but significantly increased AP lability under both NS (P = 0.001) and HS (P = 0.001). SAD did not change mean LAP but significantly increased LAP lability under both NS (SAD: 2.57 ± 0.43 vs. Sham: 1.73 ± 0.30 mmHg, P = 0.01) and HS (4.13 ± 1.18 vs. 2.45 ± 0.33 mmHg, P = 0.02). SAD markedly increased the frequency of high LAP, and SAD with HS prolonged the duration of LAP > 18 mmHg by nearly 20-fold compared with Sham (SAD + HS: 2,831 ± 2,366 vs. Sham + HS: 148 ± 248 s, P = 0.01). We conclude that baroreflex failure impairs volume tolerance and together with salt loading increases the risk of pulmonary edema even in the absence of left ventricular dysfunction. Baroreflex failure may contribute in part to the pathogenesis of HFpEF.

Practice Patterns for Outpatients With Stable Coronary Artery Disease: A Case Vignette-based Survey Among French Cardiologists

BackgroundAlthough medical management of patients with coronary artery disease (CAD) is often based on scientific guidelines, a number of everyday clinical situations are not specifically covered by recommendations or the level of evidence is low. The aim of this study was to assess practice patterns regarding routine management of patients with stable CAD. MethodsA survey comprising six questions on two clinical scenarios regarding stable CAD management was sent to 345 cardiologists from the Nord-Pas-de-Calais Region (France). We first assessed practice patterns globally and then searched for associations with physician characteristics (age, gender, sub-specialty, and type of practice). FindingsThe response rate was 92%. Regarding management of asymptomatic CAD, 86% of the cardiologists performed routine exercise testing, before which, 69% withdrew β-blockers. After a positive exercise test, 26% immediately performed coronary angiography and 67%, further imaging tests. In the absence of left ventricular dysfunction or history of myocardial infarction, routine β-blocker prescription for stable CAD was selected by 43%. When anticoagulation was needed for atrial fibrillation, 41% initiated direct oral anticoagulants rather than vitamin-K antagonists and 50% combined aspirin with anticoagulants. For recurrent stable angina in patients with known CAD, 24% performed coronary angiography directly, 49% requested a stress test, and 27% opted for medical therapy without further diagnostic testing. Age, gender of the cardiologist, academic environment, and practice of interventional cardiology were associated with certain management patterns. InterpretationWhen not guided by high-level recommendations, practice patterns for routine clinical situations in stable CAD vary considerably. Future clinical trials should address these clinical interrogations.

PT283 Prevalence of Obesity and Other Cardiovascular Risk Factors in Young Egyptian Adults

O ST E R A B ST R A C T S cardiac events compared to those with established coronary artery disease (CAD), many continue to experience chest pain. Objectives: The objective of this study is to identify the clinical determinants of recurrent chest pain at 12 months in patients with chest pain and NoCAD at the original diagnostic angiogram. Methods: Angiographic, clinical and health status (determined from the Seattle Angina Questionnaire, SAQ) details were obtained from patients undergoing diagnostic coronary angiography for evaluation of chest pain at two participating Adelaide public hospitals, between 2003-2007. NoCAD was defined as no stenosis 50% and the absence of left ventricular dysfunction, or valvular heart disease. The Thrombolysis in Myocardial Infarction (TIMI) flow grade and the corrected TIMI frame count (CTFC) were also determined from the index diagnostic angiogram. Clinical and health status details were prospectively re-assessed at 12 months following index angiography. Results: Of the 1,146 patients undergoing angiography, 320 (28%) had NoCAD. Compared with patients who had CAD, the NoCAD patients were younger (62 11 vs 57 12 years, p <0.01) and more often female (26% vs 57%, p<0.01). At 12month follow-up, ongoing chest pain was similar between CAD (59%) and NoCAD (53%, p1⁄40.10) patients. Multivariable logistic regression assessment of ongoing chest pain identified only younger age (OR1⁄40.97; 95%CI:0.95-0.99, p1⁄40.011) and female gender (OR1⁄42.34; 95%CI:1.35-4.08, p1⁄40.003) as signficant independent predictors. Conclusion: Over half of NoCAD patients continue to experience chest pain 12 months following index angiography; especially if they are younger and female, whereas the presence of conventional risk factors and angiographic findings were not important predictors. Disclosure of Interest: None Declared

Striking Volume Intolerance Is Induced by Mimicking Arterial Baroreflex Failure in Normal Left Ventricular Function

BackgroundPatients with heart failure and preserved ejection fraction (HFpEF) are supersensitive to volume overload, and a striking increase in left atrial pressure (LAP) often occurs transiently and is rapidly resolved by intravascular volume reduction. The arterial baroreflex is a powerful regulator of intravascular stressed blood volume. We examined whether arterial baroreflex failure (FAIL) mimicked by constant carotid sinus pressure (CSP) causes a striking increase in LAP and systemic arterial pressure (AP) by volume loading in rats with normal left ventricular (LV) function. Methods and ResultsIn anesthetized Sprague-Dawley rats, we isolated bilateral carotid sinuses and controlled CSP by a servo-controlled piston pump. We mimicked the normal arterial baroreflex by matching CSP to instantaneous AP and FAIL by maintaining CSP at a constant value regardless of AP. We infused dextran stepwise (infused volume [Vi]) until LAP reached 15 mm Hg and obtained the LAP-Vi relationship. We estimated the critical Vi as the Vi at which LAP reached 20 mm Hg. In FAIL, critical Vi decreased markedly from 19.4 ± 1.6 mL/kg to 15.6 ± 1.6 mL/kg (P < .01), whereas AP at the critical Vi increased (194 ± 6 mm Hg vs 163 ± 6 mm Hg; P < .01). We demonstrated that an artificial arterial baroreflex system we recently developed could fully restore the physiologic volume intolerance in the absence of native arterial baroreflex. ConclusionsArterial baroreflex failure induces striking volume intolerance in the absence of LV dysfunction and may play an important role in the pathogenesis of acute heart failure, especially in states of HFpEF.

Abstract 9675: Does the Degree of Left Ventricular Dysfunction or Symptom Status Influence the Risk of Stroke or Systemic Embolism Among Patients With Atrial Fibrillation and Heart Failure?-Results From the ACTIVE Study

Background: Heart failure (HF) is a major component of widely applied stroke risk stratification schemes in atrial fibrillation (AF). However, data regarding the relationship between left ventricular (LV) dysfunction or HF symptoms and risk of stroke/systemic embolism among HF patients remains sparse. Methods: A total of 3487 participants from the Atrial Fibrillation Clopidogrel Trial with Irbesartan for Prevention of Vascular Events (ACTIVE) trials with HF at baseline were randomized to anti-platelet therapy. Patients with HF were categorized as having preserved vs reduced ejection fraction (PEF ≥ 0.50, REF &lt; 0.50). If reduced, the degree of LV dysfunction was classified as mild, moderate or severe. HF symptoms were assessed using New York Heart Association (NYHA) class I-IV. Cox proportional-hazards models were used to estimate hazard ratios (HR, 95% CI) for stroke/systemic embolism across categories of LV dysfunction and NYHA class. Results: At baseline, 875 (47%) had HF-PEF, 982 (53%) had HF-REF; the degree of LV dysfunction was classified as mild in 25%, moderate in 25% and severe in 14%. During 3.6 years of follow-up, 211 patients had stroke/systemic embolism. In multivariable analysis, independent predictors of stroke were age ≥ 75 years (HR 2.83, 1.80-4.44), diabetes (HR 1.45, 1.03-2.03), diastolic blood pressure (per 1 mmHg, HR 1.02, 1.01-1.04), peripheral arterial disease(HR 1.94, 1.10-3.41), female(HR 1.48, 1.07-2.05) and prior stroke/transient ischemic attack (HR 1.77, 1.23-2.54) however EF &lt; 0.50, LV dysfunction or NYHA class were not predictors. Compared to those with HF-REF, patients with HF-PEF exhibited similar risk of stroke/systemic embolism: 4.18% vs. 3.83% per year, HR 0.89, 95% CI 0.65-1.22 after controlling for AF risk factors. Compared to normal LV function, there was no significant trend across categories of LV systolic dysfunction (p for trend, 0.57). The risk of stroke/systemic embolism was similar in HF patients with NYHA class I (4.0% per year, referent category), II (4.0%, HR 0.87, 0.60-1.26), III (3.9%, HR 0.62, 0.38-1.02), or IV (2.8%, 0.60, 0.14-2.55). Conclusion: Among patients with a history of HF, the presence or absence of LV dysfunction or severity of HF symptoms did not influence the risk of stroke/systemic embolism.

Association of Hyponatremia and Outcomes in Pulmonary Hypertension

BackgroundHyponatremia is known to be an important marker and prognosticator in left-sided heart failure. However, less is known about the significance of hyponatremia in pulmonary hypertension, particularly in the absence of left ventricular dysfunction. Methods and ResultsWe identified 635 patients with pulmonary hypertension and preserved ejection fraction who were normonatremic (n = 493) or hyponatremic (n = 142). End points were mortality and readmission at 1 year. Overall, 27% of all of the patients died within 1 year. Hyponatremia was significantly associated with an increased rate of 1-year mortality (hazard ratio [HR] 1.82, 95% confidence interval [CI] 1.27–2.61; P = .001) and trended toward an association with the composite of mortality and readmission (HR 1.25, 95% CI 0.97–1.62; P = .08). Additionally, the severity of hyponatremia was directly related to the rate of 1-year mortality (P < .001). ConclusionsHyponatremia is an indicator of poor prognosis in patients with echocardiographic evidence of pulmonary hypertension.

TUGENDHAT: a pilot randomized study on effects of biventricular pacing in patients with bradycardia pacing indication and normal systolic function on heart failure, atrial fibrillation and quality of life (results of 12 month follow-up)

Since the late 1990s, a growing number of clinical studies have indicated that long-term permanent right ventricular (RV) apical pacing will induce severe complications such as development of heart failure, increased burden of atrial fibrillation leading to decreased quality of life. To investigate whether cardiac resynchronization therapy (CRT) using biventricular (BiV) pacing can prevent the development of left ventricular (LV) dysfunction, LV remodelling, worsening of the clinical status and quality of life in chronically RV paced patients with normal LV ejection fraction (EF). A total of 127 patients with Class I indication for permanent cardiac pacing and without established indication for CRT were subjected to 6 months of RV and BiV pacing in a patient-blinded, randomized crossover trial. Treatment effects of BiV pacing were evaluated for LV function, LV remodelling and clinical status. As compared with RV pacing, BiV pacing did not significantly prevent the decrease of LV function [LVEF 61.0 % (36.0; 68.0) vs 60.5 % (38.5; 67.5) in RV pacing], did not change the functional class according to the New York Heart Association [52 % in Class II vs 53.9 % in Class II in RV pacing, and 3.9 % in Class III vs 6.9 % in Class III in RV pacing], and did not present any changes in quality of life [32.5 (18.0; 80.0) vs 32.0 (21.0; 47.0) indexes in RV pacing]. BiV pacing, compared to RV pacing, did not change LV function and quality of life in patients with the absence of LV dysfunction or remodelling, standard bradycardia pacing indications in a pilot phase (12- month follow-up) of the TUGENDHAT trial. The final report will be published after 60-month follow-up termination (Tab. 5, Fig. 3, Ref. 30).

A case of primary aldosteronism presenting as non-ST elevation myocardial infarction

A case of primary aldosteronism presenting as non-ST elevation myocardial infarction

Can brain natriuretic peptide predict the outcome in patients with acute pulmonary embolism?

Risk of death is high in patients with pulmonary embolism (PE) because of right ventricular (RV) failure. Plasma levels of brain natriuretic peptide (BNP) are increased in cases of isolated chronic right ventricular dysfunction (RVD) and chronic pulmonary hypertension. However, little is known about BNP secretion during acute RVD caused by acute PE.The aim of this study is to determine BNP levels in patients with acute PE with and without RVD and to assess its role in prediction of severity and outcome of these patients. Patients and methodsThis study was conducted on 47 patients with confirmed acute PE who were admitted to the intensive care unit (ICU) of Chest Department, Zagazig University Hospitals. Patients enrolled in this study were subjected to: (a) Transthoracic echocardiography, (b) Measurement of BNP plasma levels, (c) Measurement of D-dimer serum levels and d) Computed tomography pulmonary angiography (CTPA). ResultsThere was statistically highly significant increase in plasma level of BNP (pg/mL) in patients with RVD than those without it. There were highly significant positive correlations between plasma level of BNP (pg/mL) and both RV diameter (mm) and RVSP (mmHg). A plasma BNP level >72.5pg/mL can predict occurrence of RVD, while a plasma level of BNP >150pg/mL can predict death in patients with acute PE. ConclusionAn elevated plasma level of BNP is a prognostic factor for short-term mortality and overall short-term complicated clinical outcome, and it is a powerful indicator of RVD in patients with acute PE in the absence of left ventricular dysfunction (LVD).

Early Recognition and Management of Pulmonary Arterial Hypertension: ACase for Profiling

Early Recognition and Management of Pulmonary Arterial Hypertension: ACase for Profiling

Tako Tsubo syndrome: A literature review and a case report

The Tako-Tsubo syndrome is a rare yet recognized condition characterized by acute but rapidly reversible left ventricular dysfunction in absence of obstructive coronary artery stenosis. Although several factors have been associated with the development of this syndrome, still its etiology remains undefined. We report the case of a 51-years-old woman presenting with dyspnea in whom the diagnosis of Tako-Tsubo syndrome was posed. We describe the diagnostic modalities and the clinical outcome of the patient. Secondly, the present paper is aimed at providing a review of the current evidence over this topic and at proposing future research directions.

A Healthy Dose of Heavy Metal: Magnesium and Acute Lung Injury

Acute lung injury (ALI) and its more serious manifestation, acute respiratory distress syndrome (ARDS), are all too common occurrences in intensive care units around the world that create a large debt to society both in the short term [ 1 Rubenfeld G.D. Caldwell E. Peabody E. et al. Incidence and outcomes of acute lung injury. N Engl J Med. 2005; 353: 1685 Crossref PubMed Scopus (2783) Google Scholar ] and the long term [ 2 Herridge M.S. Tansey C.M. Matte A. et al. Functional disability 5 years after acute respiratory distress syndrome. N Engl J Med. 2011; 364: 1293 Crossref PubMed Scopus (1671) Google Scholar ]. These clinical syndromes claim thousands of lives each year and have been the object of many high profile studies in the past two decades. Unfortunately, despite extensive research efforts, we still have relatively little we can do to treat this condition. First described in 1967 [ 3 Ashbaugh D.G. Bigelow D.B. Petty T.L. et al. Acute respiratory distress in adults. Lancet. 1967; 2: 319 Abstract PubMed Google Scholar ] with acute dyspnea, hypoxia refractory to oxygen therapy, and diffuse lung infiltrates, the ALI/ARDS definition was further refined in 1994 by the American-European Consensus Conference on ARDS, which is still in use today. ALI requires: (1) acute onset, (2) a ratio of arterial oxygen tension to inspired oxygen concentration (PaO2/FiO2) of less than 300 mm Hg, (3) bilateral infiltrates on chest radiograph, and (4) absence of left ventricular dysfunction [ 4 Bernard G.R. Artigas A. Brigham K.L. et al. The American-European Consensus Conference on ARDSDefinitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994; 149: 818 Crossref PubMed Scopus (5235) Google Scholar ]. The definition for ARDS is the same except it requires the PaO2/FiO2 to be less than 200 mm Hg. Magnesium Sulfate Mitigates Lung Injury Induced by Bilateral Lower Limb Ischemia-Reperfusion in RatsJournal of Surgical ResearchVol. 171Issue 1PreviewLower limb ischemia-reperfusion (I/R) elicits oxidative stress and causes inflammation in lung tissues that may lead to lung injury. Magnesium sulfate (MgSO4) possesses potent anti-oxidation and anti-inflammation capacity. We sought to elucidate whether MgSO4 could mitigate I/R-induced lung injury. As MgSO4 is an L-type calcium channel inhibitor, the role of the L-type calcium channels was elucidated. Full-Text PDF

Usefulness of Pericardial Effusion as New Diagnostic Criterion for Noninvasive Detection of Myocarditis

Cardiovascular magnetic resonance (CMR) imaging holds promise for diagnosing myocarditis in vivo. The CMR diagnosis of myocarditis is determined by the ventricular morphology/function, late gadolinium enhancement, and T(2)-weighted imaging for myocardial edema. However, in routine clinical practice, we encounter patients with suspected myocarditis in the absence of left ventricular dysfunction, myocardial edema, or late gadolinium enhancement. In the present study, we sought to determine whether the presence of pericardial effusion could serve as a new diagnostic criterion and improve the sensitivity of CMR imaging to detect myocarditis. A total of 35 consecutive patients with biopsy proven virus-associated myocarditis, onset of clinical symptoms within the past 3 months, and normal left ventricular function were enrolled in the present study. All patients underwent echocardiography, CMR imaging, and endomyocardial biopsy for workup of myocarditis. Late gadolinium enhancement was present in 16 patients (46%). Myocardial edema on T(2)-weighted imaging was present in 4 patients, but in just 1, it was the only abnormal finding. Pericardial effusion was present in 14 patients (40%). In 7 patients with myocarditis (20%), pericardial effusion was the only abnormal finding. Pericardial effusion, used as an additional diagnostic criterion, improved the sensitivity of CMR imaging for myocarditis from 46% to 66% (p = 0.023). In conclusion, pericardial effusion detected by CMR imaging might serve as a new diagnostic criterion for the noninvasive diagnosis of myocarditis in patients with recent onset of clinical symptoms and normal left ventricular function.

Predictive value of plasma Nt-proBNP and body mass index for recurrence of atrial fibrillation after cardioversion

Natriuretic peptides might be useful to guide therapy in patients with atrial fibrillation (AF). B-type natriuretic peptide (BNP) is elevated in patients with AF with and without heart failure [1,2]. In the absence of left ventricular dysfunction the natriuretic peptides are mainly produced in the atria [3]. Changes of N-terminal fragment of pro-brain natriuretic peptide (Nt-proBNP) following cardioversion (CV) are less intensively investigated. Furthermore, little is known, whether changes of Nt-proBNP after CV could be used to predict recurrence of AF (re-AF).