Paul Cremer

Clinical Decision Making With Myocardial Perfusion Imaging in Patients With Known or Suspected Coronary Artery Disease

Myocardial perfusion imaging (MPI) to diagnose coronary artery disease (CAD) is best performed in patients with intermediate pretest likelihood of disease; unfortunately, pretest likelihood is often overestimated, resulting in the inappropriate use of perfusion imaging. A good functional capacity often predicts low risk, and MPI for diagnosing CAD should be reserved for individuals with poor exercise capacity, abnormal resting electrocardiography, or an intermediate or high probability of CAD. With respect to anatomy-based testing, coronary CT angiography has a good negative predictive value, but stenosis severity correlates poorly with ischemia. Therefore decision making with respect to revascularization may be limited when a purely noninvasive anatomical test is used. Regarding perfusion imaging, the diagnostic accuracies of SPECT, PET, and cardiac magnetic resonance are similar, though fewer studies are available with cardiac magnetic resonance. PET coronary flow reserve may offer a negative predictive value sufficiently high to exclude severe CAD such that patients with mild to moderate reversible perfusion defects can forego invasive angiography. In addition, combined anatomical and perfusion-based imaging may eventually offer a definitive evaluation for diagnosing CAD, even in higher risk patients. Any remarkable findings on single-photon emission computed tomography and PET MPI studies are valuable for prognostication. Furthermore, assessment of myocardial blood flow with PET is particularly powerful for prognostication as it reflects the end result of many processes that lead to atherosclerosis. Decision making with respect to revascularization is limited for cardiac MRI and PET MPI. In contrast, retrospective radionuclide studies have identified an ischemic threshold, but randomized trials are needed. In patients with at least moderately reduced left ventricular systolic function, viable myocardium as assessed by PET or MRI, appears to identify patients who benefit from revascularization, but well-executed randomized trials are lacking.

Quantitative assessment of pericardial delayed hyperenhancement predicts clinical improvement in patients with constrictive pericarditis treated with anti-inflammatory therapy.

Background—Delayed hyperenhancement (DHE) of the pericardium usually represents ongoing inflammation and may identify patients with constrictive pericarditis that will improve with anti-inflammatory therapy. However, a quantitative assessment of pericardial DHE has not been performed, and the hierarchical relationship among clinical factors, inflammatory markers, and pericardial DHE is unknown. Methods and Results—We identified 41 consecutive patients with constrictive pericarditis who had a cardiovascular magnetic resonance study with DHE prior to the initiation of anti-inflammatory medications. Pericardial inflammation was quantified on short-axis DHE sequences by contouring the pericardium, selecting normal septal myocardium as a reference region, and then quantifying the pericardial signal that was >6 SD above the reference. Our primary outcome was clinical improvement with anti-inflammatory therapy. The mean age of our patients was 58 years, most patients were male (83%) with New York Heart Association Class II or III (59%) heart failure, and the median follow-up was 1 year. Chest pain, lower New York Heart Association class, higher Westergren sedimentation rates, and increased pericardial DHE were all significantly associated with clinical improvement (P<0.01 for all). When quantitative pericardial DHE was added to a model that included age, chest pain, New York Heart Association class, and Westergren sedimentation rates, the global &khgr;2 improved significantly (P=0.04 for DHE), and the area under the receiver operating characteristic curve was 0.96. Conclusions—In patients with constrictive pericarditis treated with anti-inflammatory therapy, a quantitative assessment of pericardial DHE can provide incremental information to predict clinical improvement when added to clinical factors and Westergren sedimentation rates.

Myocardial perfusion imaging in emergency department patients with negative cardiac biomarkers: yield for detecting ischemia, short-term events, and impact of downstream revascularization on mortality.

Background—In patients with possible acute coronary syndromes, guidelines recommend routine provocative testing after negative cardiac biomarkers. We hypothesized that myocardial perfusion imaging would be low yield with limited short-term value and that early revascularization would not affect mortality. Methods and Results—We identified consecutive patients referred from our emergency department between October 2004 and September 2011 who had myocardial perfusion imaging after negative troponin T tests and nondiagnostic ECGs. We assessed the incidence of abnormal myocardial perfusion imaging, coronary angiography, revascularization, and mortality. In a cohort of 5354 patients (58.7% female, age 59±13, 78.6% thrombolysis in myocardial infarction [TIMI] ⩽2), 9% had >5% and 3.6% had >10% ischemic myocardium. Among patients with TIMI scores ⩽2, 6.1% had >5% ischemic myocardium compared with 19.6% of patients with TIMI scores ≥3 (P<0.001). At 30 days, 7 patients were deceased, 187 had revascularization, and 6 had revascularization for an acute myocardial infarction. Over 3.4±1.9 years of follow-up, 347 patients died. In propensity-matched groups of patients with ischemia, there was no association between early revascularization and mortality (hazard ratio, 1.00; 95% confidence interval, 0.49–2.07). Conclusions—Routine provocative testing to detect ischemia before emergency department discharge is low yield in patients with negative troponins and TIMI scores ⩽2 and modest yield in patients with TIMI scores ≥3. In all patients, 30 days events are rare. Finally, in patients with ischemia, we are unable to demonstrate a mortality benefit with early revascularization.

Early Bioprosthetic Valve Failure: Mechanistic Insights via Correlation between Echocardiographic and Operative Findings

Bioprosthetic valves are increasingly implanted, with generally consistent and durable results. Early bioprosthetic valve failure is uncommon, and most clinicians are unfamiliar with the spectrum of early structural complications involving bioprostheses. In this review, the authors organize causes of early bioprosthetic valve failure according to possible pathogenesis, demonstrate the correlation between echocardiographic and anatomic findings, and discuss potential treatments. First, they address early bioprosthetic valve stenosis secondary to thrombosis. Next, they discuss excessive pannus formation, a hitherto rarely described cause of early bioprosthetic valve failure. Finally, the authors address early structural valve deterioration mediated by calcification or primary tears. Illustrative examples with relevant echocardiographic and operative findings are provided.

Multimodality Imaging of Pericardial Disease

The emergence of multimodality imaging of pericardial diseases has improved diagnosis and management. In acute pericarditis, echocardiography is the first-line test, but cardiac magnetic resonance (CMR) may be beneficial in patients who fail to respond to therapy. An increased T2 short-tau inversion recovery time (STIR) suggests pericardial edema, and increased late gadolinium enhancement (LGE) suggests organizing pericarditis. Computed tomography (CT) can be helpful in procedural planning, either to guide percutaneous drainage of an effusion or to assess calcification and the location of vascular structures before pericardiectomy. On echocardiography, a respiratory septal shift in combination with either a preserved medial e′ velocity or prominent expiratory diastolic hepatic vein flow reversal performs well in diagnosing constrictive pericarditis. These patients also have decreased regional longitudinal strain in the anterolateral and right ventricular free walls, presumably related to pericardial to myocardial tethering. Finally, prominent LGE may identify patients with constrictive pericarditis who improve with anti-inflammatory therapy.

Reliability of updated left ventricular diastolic function recommendations in predicting elevated left ventricular filling pressure and prognosis

Background An updated 2016 echocardiographic algorithm for diagnosing left ventricular (LV) diastolic dysfunction (DD) was recently proposed. We aimed to assess the reliability of the 2016 echocardiographic LVDD grading algorithm in predicting elevated LV filling pressure and clinical outcomes compared to the 2009 version. Methods We retrospectively identified 460 consecutive patients without atrial fibrillation or significant mitral valve disease who underwent transthoracic echocardiography within 24 hours of elective heart catheterization. LV end‐diastolic pressure (LVEDP) and the time constant of isovolumic pressure decay (Tau) were determined. The association between DD grading by 2009 LVDD Recommendations and 2016 Recommendations with hemodynamic parameters and all‐cause mortality were compared. Results The 2009 LVDD Recommendations classified 55 patients (12%) as having normal, 132 (29%) as grade 1, 156 (34%) as grade 2, and 117 (25%) as grade 3 DD. Based on 2016 Recommendations, 177 patients (38%) were normal, 50 (11%) were indeterminate, 124 (27%) patients were grade 1, 75 (16%) were grade 2, 26 (6%) were grade 3 DD, and 8 (2%) were cannot determine. The 2016 Recommendations had superior discriminatory accuracy in predicting LVEDP (P < .001) but were not superior in predicting Tau. During median follow‐up of 416 days (interquartile range: 5 to 2004 days), 54 patients (12%) died. Significant DD by 2016 Recommendations was associated with higher risk of mortality (P = .039, subdistribution HR1.85 [95% CI, 1.03‐3.33]) in multivariable competing risk regression. Conclusions The grading algorithm proposed by the 2016 LV diastolic dysfunction Recommendations detects elevated LVEDP and poor prognosis better than the 2009 Recommendations.

New Insights into Pericarditis: Mechanisms of Injury and Therapeutic Targets

Purpose of ReviewThis review article aims to provide a contemporary insight into the pathophysiological mechanisms of and therapeutic targets for pericarditis, drawing distinction between autoinflammatory and autoimmune pericarditis.Recent FindingsRecent research has focused on the distinction between autoinflammatory and autoimmune pericarditis. In autoinflammatory pericarditis, viruses can activate the sensor molecule of the inflammasome, which results in downstream release of cytokines, such as interleukin-1, that recruit neutrophils and macrophages to the site of injury. Conversely, in autoimmune pericarditis, a type I interferon signature predominates, and pericardial manifestations coincide with the severity of the underlying systemic autoimmune disease. In addition, autoimmune pericarditis can also develop after cardiac injury syndromes. With either type of pericarditis, imaging can help stage the inflammatory state. Prominent pericardial delayed hyperenhancement on magnetic resonance imaging suggests ongoing inflammation whereas calcium on computed tomography suggests a completed inflammatory cascade. In patients with ongoing pericarditis, treatments that converge on the inflammasome, such as colchicine and anakinra, have proved effective in recurrent autoinflammatory pericarditis, though further clinical trials with anakinra are warranted.SummaryAn improved understanding of the pathophysiological mechanisms of pericarditis helps unravel effective therapeutic targets for this condition.

Pericardial Effusions: Causes, Diagnosis, and Management.

The presentation of a patient with a pericardial effusion can range from an incidental finding to a life-threatening emergency. Accordingly, the causes of pericardial effusions are numerous and can generally be divided into inflammatory and non-inflammatory etiologies. For all patients with a suspected pericardial effusion, echocardiography is essential to define the location and size of an effusion. In pericardial tamponade, the hemodynamics relate to decreased pericardial compliance, ventricular interdependence, and an inspiratory decrease in the pressure gradient for left ventricular filling. Echocardiography provides insight into the pathophysiologic alterations, primarily through an assessment of chamber collapse, inferior vena cava plethora, and marked respiratory variation in mitral and tricuspid inflow. Once diagnosed, pericardiocentesis is performed in patients with tamponade, preferably with echocardiographic guidance. With a large effusion but no tamponade, pericardiocentesis is rarely needed for diagnostic purposes, though is performed if there is concern for a bacterial infection. In patients with malignancy, pericardial window is preferred given the risk for recurrence. Finally, large effusions can progress to tamponade, but can generally be followed closely until the extent of the effusion facilitates safe pericardiocentesis.

Three mechanisms of early failure of transcatheter aortic valves: Valve thrombosis, cusp rupture, and accelerated calcification

From the Robert and Suzanne Tomisch Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio. Disclosures: Authors have nothing to disclose with regard to commercial support. Received for publication Nov 3, 2016; revisions received Nov 30, 2016; accepted for publication Dec 6, 2016; available ahead of print Jan 7, 2017. Address for reprints: Matthew R. Summers, MD, Robert and Suzanne Tomisch Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, J1-5 9500 Euclid Ave, Cleveland, OH 44195 (E-mail: summerm3@ccf.org). J Thorac Cardiovasc Surg 2017;153:e87-93 0022-5223/

Use of Sex-Specific Clinical and Exercise Risk Scores to Identify Patients at Increased Risk for All-Cause Mortality

36.00 Copyright 2016 by The American Association for Thoracic Surgery http://dx.doi.org/10.1016/j.jtcvs.2016.12.011 TTE of a distinct mechanism of early TAVR failure: thrombosis.