Abnormal Myocardial Blood Flow Reserve Observed in Cardiac Amyloidosis

We performed real-time myocardial contrast echocardiography on a patient with cardiac amyloidosis and previous normal coronary angiography presenting with atypical chest pain to assess myocardial blood flow reserve (MBFR). Myocardial contrast echocardiography was performed and flash microbubble destruction and replenishment analysis was used to calculate myocardial blood flow. Dipyridamole was used to achieve hyperemia. MBFR was derived from the ratio of peak myocardial blood flow at hyperemia and rest. The results show a marked reduction in MBFR in our patient. Previous reports of luminal obstruction of intramyocardial rather than epicardial vessels by amyloid deposition may be causing microvascular dysfunction

Lactate concentration gradient from right atrium to pulmonary artery: a commentary

Inadequate myocardial performance is a common complication of severe sepsis. Studies in humans strongly argue against a decrease in coronary blood flow in the pathogenesis of this sepsis-induced cardiac injury. Moreover, regional myocardial ischemia may well be present in sepsis patients with coexistent coronary artery disease. Nevertheless, the diagnosis of myocardial ischemia remains difficult in patients with sepsis, since elevation of troponin in these patients can be the result of a variety of conditions other than acute myocardial ischemia. The use of the right atrium to pulmonary artery lactate gradient could perhaps help the clinician in detecting myocardial ischemia in patients with sepsis

Myocardial dysfunction after out-of-hospital cardiac arrest: predictors and prognostic implications.

We aim to determine the incidence of early myocardial dysfunction after out-of-hospital cardiac arrest, risk factors associated with its development, and association with outcome. A retrospective chart review was performed among consecutive out-of-hospital cardiac arrest (OHCA) patients who underwent echocardiography within 24 h of return of spontaneous circulation at three urban teaching hospitals. Our primary outcome is early myocardial dysfunction, defined as a left ventricular ejection fraction \u3c 40% on initial echocardiogram. We also determine risk factors associated with myocardial dysfunction using multivariate analysis, and examine its association with survival and neurologic outcome. A total of 190 patients achieved ROSC and underwent echocardiography within 24 h. Of these, 83 (44%) patients had myocardial dysfunction. A total of 37 (45%) patients with myocardial dysfunction survived to discharge, 39% with intact neurologic status. History of congestive heart failure (OR 6.21; 95% CI 2.54-15.19), male gender (OR 2.27; 95% CI 1.08-4.78), witnessed arrest (OR 4.20; 95% CI 1.78-9.93), more than three doses of epinephrine (OR 6.10; 95% CI 1.12-33.14), more than four defibrillations (OR 4.7; 95% CI 1.35-16.43), longer duration of resuscitation (OR 1.06; 95% CI 1.01-1.10), and therapeutic hypothermia (OR 3.93; 95% CI 1.32-11.75) were associated with myocardial dysfunction. Cardiopulmonary resuscitation immediately initiated by healthcare personnel was associated with lower odds of myocardial dysfunction (OR 0.40; 95% CI 0.17-0.97). There was no association between early myocardial dysfunction and mortality or neurological outcome. Nearly half of OHCA patients have myocardial dysfunction. A number of clinical factors are associated with myocardial dysfunction, and may aid providers in anticipating which patients need early diagnostic evaluation and specific treatments. Early myocardial dysfunction is not associated with neurologically intact survival

Spatio-Temporal Modelling of Perfusion Cardiovascular MRI

Myocardial perfusion MRI provides valuable insight into how coronary artery and microvascular diseases affect myocardial tissue. Stenosis in a coronary vessel leads to reduced maximum blood flow (MBF), but collaterals may secure the blood supply of the myocardium but with altered tracer kinetics. To date, quantitative analysis of myocardial perfusion MRI has only been performed on a local level, largely ignoring the contextual information inherent in different myocardial segments. This paper proposes to quantify the spatial dependencies between the local kinetics via a Hierarchical Bayesian Model (HBM). In the proposed framework, all local systems are modelled simultaneously along with their dependencies, thus allowing more robust context-driven estimation of local kinetics. Detailed validation on both simulated and patient data is provided

Prognostic value of the myocardial salvage index measured by T2-weighted and T1-weighted late gadolinium enhancement magnetic resonance imaging after ST-segment elevation myocardial infarction: A systematic review and meta-regression analysis

In all patients with ST-segment elevation myocardial infarction, risk stratification should be performed before discharge. The measurement of therapy efficiency with magnetic resonance imaging has been proposed as part of the risk assessment, but it has not been adopted widely. This meta-analysis was conducted to summarize published data on the prognostic value of the proportion of salvaged myocardium inside previously ischemic myocardium (myocardial salvage index) measured by T2-weighted and T1-weighted late gadolinium enhancement magnetic resonance imaging after ST-segment elevation myocardial infarction. Random and mixed effects models were used for analyzing the data of 10 studies with 2,697 patients. The pooled myocardial salvage index, calculated as the proportion of non-necrotic myocardium inside edematous myocardium measured by T2-weighted and T1-weighted late gadolinium enhancement MRI, was 43.0% (95% confidence interval: 37.4, 48.6). The pooled length of follow-up was 12.3 months (95% confidence interval: 7.0, 17.6). The pooled incidence of major cardiac events during follow-up, defined as cardiac death, nonfatal myocardial infarction, or admission for heart failure, was 10.6% (95% confidence interval: 5.7, 15.5). The applied mixed effects model showed an absolute decrease of 1.7% in the incidence of major cardiac events during follow-up (95% confidence interval: 1.6, 1.9) with every 1% of increase in the myocardial salvage index. The heterogeneity between studies was considerable (τ = 21.3). Analysis of aggregated follow-up data after ST-segment elevation myocardial infarction suggests that the myocardial salvage index measured by T2-weighted and T1-weighted late gadolinium enhancement magnetic resonance imaging provides prognostic information on the risk of major cardiac events, but considerable heterogeneity exists between studies

Combination GLP-1 and Insulin Treatment Fails to Alter Myocardial Fuel Selection Versus Insulin Alone in Type 2 Diabetes

Context Glucagon-like peptide-1 (GLP-1) and the clinically available GLP-1 agonists have been shown to exert effects on the heart. It is unclear whether these effects occur at clinically used doses in vivo in humans, possibly contributing to CVD risk reduction. Objective To determine whether liraglutide at clinical dosing augments myocardial glucose uptake alone or in combination with insulin compared to insulin alone in metformin-treated Type 2 diabetes mellitus. Design Comparison of myocardial fuel utilization after 3 months of treatment with insulin detemir, liraglutide, or combination detemir+liraglutide. Setting Academic hospital Participants Type 2 diabetes treated with metformin plus oral agents or basal insulin. Interventions Insulin detemir, liraglutide, or combination added to background metformin Main Outcome Measures Myocardial blood flow, fuel selection and rates of fuel utilization evaluated using positron emission tomography, powered to demonstrate large effects. Results We observed greater myocardial blood flow in the insulin-treated groups (median[25th, 75th percentile]: detemir 0.64[0.50, 0.69], liraglutide 0.52[0.46, 0.58] and detemir+liraglutide 0.75[0.55, 0.77] mL/g/min, p=0.035 comparing 3 groups and p=0.01 comparing detemir groups to liraglutide alone). There were no evident differences between groups in myocardial glucose uptake (detemir 0.040[0.013, 0.049], liraglutide 0.055[0.019, 0.105], detemir+liraglutide 0.037[0.009, 0.046] µmol/g/min, p=0.68 comparing 3 groups). Similarly there were no treatment group differences in measures of myocardial fatty acid uptake or handling, and no differences in total oxidation rate. Conclusions These observations argue against large effects of GLP-1 agonists on myocardial fuel metabolism as mediators of beneficial treatment effects on myocardial function and ischemia protection

Computational modeling of acute myocardial infarction

This is an Accepted Manuscript of an article published by Taylor & Francis Group in Computer Methods in Biomechanics and Biomedical Engineering on October, 2016, available online at: http://www.tandfonline.com/10.1080/10255842.2015.1105965Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size.Peer ReviewedPostprint (author's final draft

Which diagnostic tests are most useful in a chest pain unit protocol?

Background The chest pain unit (CPU) provides rapid diagnostic assessment for patients with acute, undifferentiated chest pain, using a combination of electrocardiographic (ECG) recording, biochemical markers and provocative cardiac testing. We aimed to identify which elements of a CPU protocol were most diagnostically and prognostically useful. Methods The Northern General Hospital CPU uses 2–6 hours of serial ECG / ST segment monitoring, CK-MB(mass) on arrival and at least two hours later, troponin T at least six hours after worst pain and exercise treadmill testing. Data were prospectively collected over an eighteen-month period from patients managed on the CPU. Patients discharged after CPU assessment were invited to attend a follow-up appointment 72 hours later for ECG and troponin T measurement. Hospital records of all patients were reviewed to identify adverse cardiac events over the subsequent six months. Diagnostic accuracy of each test was estimated by calculating sensitivity and specificity for: 1) acute coronary syndrome (ACS) with clinical myocardial infarction and 2) ACS with myocyte necrosis. Prognostic value was estimated by calculating the relative risk of an adverse cardiac event following a positive result. Results Of the 706 patients, 30 (4.2%) were diagnosed as ACS with myocardial infarction, 30 (4.2%) as ACS with myocyte necrosis, and 32 (4.5%) suffered an adverse cardiac event. Sensitivities for ACS with myocardial infarction and myocyte necrosis respectively were: serial ECG / ST segment monitoring 33% and 23%; CK-MB(mass) 96% and 63%; troponin T (using 0.03 ng/ml threshold) 96% and 90%. The only test that added useful prognostic information was exercise treadmill testing (relative risk 6 for cardiac death, non-fatal myocardial infarction or arrhythmia over six months). Conclusion Serial ECG / ST monitoring, as used in our protocol, adds little diagnostic or prognostic value in patients with a normal or non-diagnostic initial ECG. CK-MB(mass) can rule out ACS with clinical myocardial infarction but not myocyte necrosis(defined as a troponin elevation without myocardial infarction). Using a low threshold for positivity for troponin T improves sensitivity of this test for myocardial infarction and myocardial necrosis. Exercise treadmill testing predicts subsequent adverse cardiac events