Amount Of Ischemic Myocardium Research Articles

Design and rationale of the efficacy of spinal cord stimulation in patients with refractory angina pectoris (SCRAP) trial.

The use of spinal cord stimulation (SCS) in patients with refractory angina pectoris (RAP) is still under debate. Studies up to date have shown a positive effect with an improvement in quality of life. However, no double blinded randomized controlled trials have been performed. The objective of this trial is to investigate if high density SCS leads to a significant reduction in the amount of myocardial ischemia in patients with RAP. Eligible patients must meet the criteria for RAP, have proven ischemia and a positive transcutaneous electrical nerve stimulator treadmill test. Patients who meet the inclusion criteria will receive an implanted spinal cord stimulator. Patients receive 6 months of high density SCS and 6 months of no stimulation using a cross-over design. The order of the treatment options is determined using randomization. The primary endpoint is the effect of SCS measured by the change in percentage of myocardial ischemia using myocardial perfusion positron emission tomography scan. Key secondary endpoints are patient related outcome measures, major cardiac adverse events and safety endpoints. The follow-up period is 1 year for the primary and key secondary endpoints. The SCRAP trial began enrollment on December 21, 2021 and is set to complete the primary assessments in June 2025. To date, January 2, 2023, 18 patients have been enrolled in the study and 3 patients have completed the 1-year follow-up. The SCRAP trial is an investigator-initiated, single-center, double-blind, placebo-controlled, and cross-over randomized controlled trial investigating the efficacy of SCS in patients with RAP. (ClinicalTrials. gov Identifier: NCT04915157).

Fractal structure of cardiovascular system

The structure of different systems, aiming to supply a volume of definite tissue with a specific fluid, which is for example the blood in the vascular system, obeys on similar lows, which can be expressed by mathematical equations. Those systems have fractal structure, that means every small part of the system repeats the structure of entire system. Knowing those dependencies permits calculation of one particular parameter of cardiovascular system, for example, the amount of myocardium on the basis of diameter of coronary artery supplying it. This approach is extremely applicable to the patients with coronary artery disease, where the amount of ischemic myocardium is of paramount importance for the patient`s fate. The aim of the current review is to present the main interdependencies between anatomical and physiological parameters of cardiovascular system.

The Relationship Between Ischaemia on Myocardial Perfusion Imaging and Chest Pain or Electrocardiogram Changes During Exercise

Background: Stress myocardial perfusion imaging (MPI) has established superior sensitivity and specificity to exercise electrocardiogram (ECG) in diagnosing myocardial ischaemia. However, the impact of chest pain or ECG changes during MPI remains unclear. This study aimed to define the relationship between chest pain or ischaemic ECG changes during MPI and the amount of myocardial ischaemia.

Correlation of Fractional Flow Reserve With Ischemic Burden Measured by Cardiovascular Magnetic Resonance Perfusion Imaging

Cardiovascular magnetic resonance (CMR) perfusion imaging and fractional flow reserve (FFR) assess myocardial ischemia. FFR measures the pressure loss across a stenosis determining hemodynamic significance but does not assess the area subtended by the stenotic vessel. CMR perfusion imaging measures the extent of myocardial blood flow reduction (=ischemic burden). Both techniques allow for continuous rather than categorical evaluation, but their relationship is poorly understood. This study investigates the relationship between the FFR value and the extent of myocardial ischemia. Forty-nine patients with angina underwent CMR perfusion imaging. FFR was measured in vessels with a visual diameter stenosis >40%. The extent of ischemia for each coronary artery was measured by delineating the perfusion defect on the CMR images and expressing as a percentage of the left ventricular myocardium. The correlation between the extent of ischemia measured by CMR and FFR was good (r = -0.85, p < 0.0005). The mean FFR value was 0.67 ± 0.17, and the mean perfusion defect was 8.9 ± 9.3%. An FFR value of ≥0.75 was not associated with ischemia on CMR. The maximum amount of ischemia (23.0 ± 1.5%) was found at FFR values 0.4 to 0.5. In patients with 1 vessel disease (49%), the mean ischemic burden was 15.3 ± 8.3%. In patients with 2 vessel diseases (18%), the mean ischemic burden was 26.0 ± 12%. Reproducibility for the measurement of ischemic burden was very good with a Kappa coefficient (k = 0.826, p = 0.048). In conclusion, there is good correlation between the FFR value and the amount of myocardial ischemia in the subtended myocardium.

Myocardial Ischemia on Exercise Stress Echocardiography Testing Is Not Associated with Changes in Troponin T Concentrations.

Some posit that any amount of myocardial ischemia can be detected by high-sensitivity cardiac troponin assays. We hypothesized that patients with myocardial ischemia induced by exercise stress would have significantly higher increases in high-sensitivity cardiac troponin T (hs-cTnT) concentrations than patients without ischemia. We prospectively recruited for a biorepository 317 adult patients who presented to an academic hospital emergency department for evaluation possible ischemic symptoms and who were scheduled for exercise echocardiography. Blood samples were obtained before stress testing and 2-h post-testing. For this study, plasma hs-cTnT (Roche Diagnostics) concentrations were determined in a core laboratory blinded to clinical status. Absolute and relative changes between baseline and 2-h post-stress measurements were compared between patients with and without ischemia induced by stress testing. The median age was 51 (44.0, 60.0) years, 45.9% were male, and 37.8% were African American. In total, 26 patients (8.1%) had myocardial ischemia induced by exercise. Median baseline, 2-h post-stress, and absolute δ concentrations were, respectively, 6.0, 8.0, and 0.2 ng/L for patients with evidence of ischemia; 3.8, 4.6, and 0.0 ng/L for those without; and 3.9, 4.9, and 0.0 ng/L overall. Baseline and 2-h hs-cTnT concentrations were higher among patients with abnormal stress tests (all P ≤0.05), but absolute and relative changes in hs-cTnT concentrations were not significantly different between individuals with ischemia and individuals without. There was no evidence of change in hs-cTnT values in response to exercise stress testing, regardless of the presence of myocardial ischemia.

(F)Utility of invasive haemodynamic measurements to guide percutaneous intervention in chronic coronary artery disease.

Percutaneous coronary intervention (PCI) in chronic stable coronary artery disease has not been shown to reduce the incidence of myocardial infarction or death. There is, however, evidence that the outcome from PCI is dependent on the amount of myocardial ischaemia. This review provides an overview of coronary circulatory pathophysiology and focuses on fractional flow reserve from a semantical, conceptual and practical point of view.

Fractional flow reserve and the correlation with ischaemic burden measured by cardiovascular magnetic resonance perfusion imaging

Objectives To investigate the relationship between the Fractional Flow Reserve (FFR) value in a coronary territory and the extent of myocardial ischaemia measured by high resolution Cardiovascular Magnetic Resonance Imaging (CMR) scanning Methods: 49 patients with angina and known or suspected coronary artery disease (CAD) referred for coronary angiography also underwent CMR perfusion imaging. FFR was measured in all vessels with a stenosis of >50%. The extent of ischaemia (both global and individual arterial territories) was measured as a percentage of the LV myocardium on CMR imaging. Interstudy reproducibility of the measurements of ischaemia was also assessed. Results: The correlation between the extent of ischaemia on a per vessel basis measured by CMR and the FFR value was good (r= -0.854, p<0.0005) An FFR value of 0.75 or above in a coronary artery was associated with no myocardial ischaemia. The maximum amount of ischaemia (mean value 23.0% (±1.5) was demonstrated at FFR values between 0.4 and 0.5. The mean value for global ischaemic burden was 12.69% (±12%). In patients with one vessel disease (49%) the mean value for percentage ischaemia was 15.3% (±8.3%). In patients with 2 vessel disease (18%) the mean value was 26% (±12%). Reproducibility for measurement of ischaemic burden was very good with a Kappa coefficient (k=0.826, p=0.048). ![Figure][1] FFR values and % ischaemia per vessel Conclusions: There is good correlation between the FFR value within a coronary artery and the amount of myocardial ischaemia caused. Relating the amount of ischaemia to the FFR value could lead to more targeted revascularisation to reduce ischaemic burden, potentially resulting in improved patient outcome. [1]: pending:yes

Spontaneous Coronary Artery Dissection Mimicking Coronary Spasm Diagnosed by Intravascular Ultrasonography

Spontaneous coronary artery dissection (SCAD) is a rare and occasionally life-threatening cause of acute coronary syndrome. Patients may present with clinical scenarios ranging from angina pectoris to cardiogenic shock to sudden cardiac death, and it may be a potentially life-threatening condition if not recognized. However, its etiology, pathophysiology and optimal therapeutic strategies have not been well understood. SCAD is diagnosed on the basis of coronary angiography, but complementary techniques as such intravascular ultrasound (IVUS) and optical coherence tomography should be considered for diagnostic clarification where appropriate. Likewise, the selection of treatment strategy depends upon the clinical manifestation, location and the extent of dissection and amount of ischemic myocardium at risk. Herein, we present the case of a 35-year-old woman who presented with acute myocardial infarction. She was diagnosed by IVUS with spontaneous diffuse dissection of the left anterior descending artery without atheroma, treated with percutaneous coronary stenting, and had a favorable clinical course and was discharged on medical therapy.

Quantification of the ischemic burden on cardiac magnetic resonance perfusion maps by perfusion threshold analysis

Background High-resolution quantitative analysis of myocardial blood flow (MBF) by cardiac magnetic resonance (CMR) perfusion has been recently proposed and validated in preclincal studies. It aims to combine the advantages of both visual assessment and quantitative analysis in a single test. However, incorrect registration between stress and rest images can hamper myocardial perfusion reserve (MPR) calculation from high-resolution perfusion maps. The aim of this study was to test the feasibility of MPR analysis from high-resolution perfusion maps as well as to test MBF threshold analysis, a novel analysis approach capable to measure the extent of ischemic myocardium with high spatial accuracy. Methods Ten patients with single-vessel coronary artery disease (CAD) and ten control subjects were analyzed at 3 Tesla. Perfusion data were analyzed on high-resolution maps and at segmental level to simulate MPR for variable degrees of image misregistration. MBF threshold analysis was then applied to high-resolution perfusion maps. In analogy to one of the methods currently in use for the quantification of late gadolinium enhancement, pixels with abnormally reduced coronary flow reserve were defined on the basis of the average MBF in areas with visually normal perfusion. In this exploratory analysis, the ischemic myocardium was defined as pixels with MBF reduced below the 90th, 95th and 99th percentile of the average epicardial MBF of the reference segment. MBF threshold analysis defines the amount of ischemic myocardium as a percentage of the LV (global ischemic burden) or of a perfusion territory (territorial ischemic burden).

Comparison of intracoronary and transendocardial delivery of allogeneic mesenchymal cells in a canine model of acute myocardial infarction

This study assessed safety of transendocardial (TE) electromechanical-guided delivery of bone marrow mesenchymal stem cells (MSCs) after acute myocardial infarction (AMI) and compared intracoronary (IC) delivery with TE delivery. In a canine acute myocardial ischemia model, 100×106 MSCs were delivered 7 days after AMI via IC and TE routes. Functional assessment was performed by 2D echocardiogram, and detailed histopathologic analyses were performed to assess the impact of cell therapy in vascular density and fibrosis. Patterns of cell distribution in both delivery methods were also compared. There was a statistically significant reduction in the amount of myocardial ischemia in the TE group (P=0.007). Left ventricular ejection fraction (LVEF) increased 13% (mean) in the TE group (21-day follow-up) and was significantly better than that of the controls (P=0.01), but did not improve in the IC-delivery group. Dissimilar patterns of cell distribution were noted between the IC and TE groups. This study suggests that MSC treatment is probably safe and effective after AMI. In the comparison of TE and IC delivery, the TE group showed higher cell retention (clusters even in the injury center of the infarct) with an increased vascularity and greater functional improvement than did the IC group (no clusters; cells at the border of the infarct). The higher local cell density in the TE group may be important for therapeutic effectiveness.

Metabolic Therapy for Patients with Diabetes Mellitus and Coronary Artery Disease

Patients with diabetes mellitus and ischemic heart disease more frequently develop heart failure and have a greater amount of myocardial ischemia, often silent, compared with patients without diabetes. Furthermore, patients with coronary artery disease (CAD) and diabetes or insulin resistance have altered myocardial metabolism and accelerated and diffuse atherogenesis with involvement of distal coronary segments that causes chronic hypoperfusion and hibernation. Therefore, in patients with diabetes and CAD, the ischemic metabolic changes are heightened by the metabolic changes in patients with diabetes. An important metabolic alteration in patients with diabetes is the increase in free fatty acid (FFA) concentrations and the increased skeletal muscle and myocardial FFA uptake and oxidation. The increased uptake and utilization of FFA and the reduced utilization of glucose as a source of energy during stress and ischemia contribute to the increased susceptibility of diabetic hearts to myocardial ischemia and to a greater decrease of myocardial performance for a given amount of ischemia compared with nondiabetic hearts. A therapeutic approach aimed at an improvement in cardiac metabolism through manipulations of the use of metabolic substrates should result in an improvement in myocardial ischemia and left ventricular (LV) function. The inhibition of FFA oxidation with trimetazidine improves cardiac metabolism at rest, increases cardiac resistance to ischemia, and therefore reduces the decrease of LV function caused by chronic hypoperfusion and repetitive episodes of myocardial ischemia in patients with and without diabetes. Thus, modulation of myocardial FFA metabolism should be the key target for metabolic interventions in patients with CAD with and without diabetes. In patients with diabetes, the effects of modulation of FFA metabolism should be even greater compared with those observed in patients without diabetes. Because of its effect on cardiac metabolism at rest and its effects on myocardial ischemia and LV function, trimetazidine should always be considered for the treatment of patients with diabetes with CAD with or without LV dysfunction.

Metabolic therapy for the diabetic patients with ischaemic heart disease

Diabetic patients with ischaemic heart disease have a greater amount of myocardial ischaemia, often silent, and an increased incidence of heart failure compared to nondiabetic patients. This is the result of altered myocardial metabolism and accelerated atherogenesis with involvement of peripheral coronary segments causing chronic hypoperfusion and diffuse hybernation. In patients with diabetes mellitus and myocardial ischaemia, the metabolic changes occurring as a consequence of the mismatch between blood supply and cardiac metabolic requirements are heightened by the diabetic metabolic changes. An important metabolic alteration of diabetes is the increase in free fatty acid concentrations and increased muscular and myocardial free fatty acid uptake and oxidation. This increased uptake and utilization of free fatty acid during stress and ischaemia is responsible for the increased susceptibility of the diabetic heart to myocardial ischaemia and to a greater decrease of myocardial performance for a given amount of ischaemia compared to nondiabetic hearts. Given the metabolic alterations of the diabetic heart at rest and during episodes of myocardial ischaemia, a therapeutic approach aimed at an improvement of cardiac metabolism through manipulations of the utilization of metabolic substrates should result in an improvement of myocardial ischaemia and of left ventricular function. Modulation of myocardial free fatty acid metabolism should be the key target for metabolic interventions in patients with coronary artery disease with and without diabetes. In diabetic patients, the effects of modulation of free fatty acid metabolism should be even greater than those observed in patients without diabetes. The inhibition of FFA oxidation with trimetazidine improves cardiac metabolism at rest, decreases cardiac ischaemia and therefore prevents the decline of left ventricular function due to chronic hypoperfusion and repetitive episodes of myocardial ischaemia. Because of its effect on cardiac metabolism at rest, its effects on myocardial ischaemia and left ventricular function trimetazidine should always be considered for the treatment of diabetic patients with ischaemic heart disease with or without left ventricular dysfunction.

Spontaneous coronary artery dissection.

Spontaneous coronary artery dissection (SCAD) is an unusual cause of acute myocardial ischemia with complex pathophysiology. This paper reviews the major diagnostic and therapeutic issues of this rare but important disease. The diagnosis of SCAD should be strongly considered in any patient who presents with symptoms suggestive of acute myocardial ischemia, particularly in young subjects without traditional risk factors for coronary artery disease (especially in young women during the peripartum period or in association with oral contraceptive use). Urgent coronary angiography is indicated to establish the diagnosis and to determine the appropriate therapeutic approach. The decision to pursue medical management, percutaneous coronary intervention, or surgical revascularization is based primarily on the clinical presentation, extent of dissection, and amount of ischemic myocardium at risk.

Long-term survival of patients with coronary artery disease and left ventricular dysfunction: Implications for the role of myocardial viability assessment in management decisions

Objectives: Our purpose was to evaluate the long-term benefit of myocardial viability assessment for stratifying risk and selecting patients with low ejection fraction for coronary artery bypass grafting and to determine the relation between the severity of anginal symptoms, the amount of ischemic myocardium, and clinical outcome. Methods: We studied 93 consecutive patients with severe coronary artery disease and low ejection fraction (median, 25%) who underwent positron emission tomography to delineate the extent of perfusion-metabolism mismatch (reflecting hibernating myocardium) for potential myocardial revascularization. Median follow-up was 4 years (range, 0 to 6.2 years). Results: Fifty patients received medical therapy, and 43 patients underwent bypass grafting. In Cox survival models, heart failure class, prior myocardial infarction, and positron emission tomographic mismatch were the best predictors of survival. Patients with positron emission tomographic mismatch receiving bypass grafting had improved 4-year survival compared with those on medical therapy (75% versus 30%; P = .007) and a significant improvement in angina and heart failure symptoms. In patients without positron emission tomographic mismatch, bypass grafting tended to improve survival and symptoms only in those patients with severe angina (100% versus 60%; P = .085), whereas no survival advantage was apparent in patients with minimal or no anginal symptoms (63% versus 52%; P = .462). Conclusions: Patients with low ejection fraction and evidence of viable myocardium by positron emission tomography have improved survival and symptoms with coronary bypass grafting compared with medical therapy. In patients without evidence of viability, survival and symptom improvement with bypass grafting are apparent only among those patients with severe angina. (J Thorac Cardiovasc Surg 1998; 116:997-1004)

Estimating ischemic burden: comparison of two formulas

Complex formulas based on elevations of the ST segment on the ECG allow noninvasive estimation of ischemic burden. However, the formulas require elaborate computations that make them clinically useless, particularly in critical and emergent situations. Estimation of the amount of ischemic myocardium is useful in monitoring effects of therapeutic interventions. To compare a simplified formula that sums ST-segment deviations in 12 ECG leads with formulas widely validated in clinical trials: anterior ischemic area = 3[1.5(number of leads ST increases) -0.4]; inferior ischemic area = 3[0.6(sigma ST increases II, III, aVF) +2.0]. Data were collected from 46 patients undergoing angioplasty of the left anterior descending branch of the coronary artery or the right coronary artery who had changes in the ST segment denoting ischemia during balloon inflation. Absolute values of ST-segment elevations or depressions in the 12 standard ECG leads with a minimum deviation of 0.5 mm were added to determine the sum of the ST-segment deviations during ischemia of the left anterior descending branch of the coronary artery and ischemia of the right coronary artery. This sum was compared with the anterior and inferior ischemic area scores. The Pearson Product-Moment Correlation Coefficient was used to measure the association between the scores. The sum of ST-segment deviations for the left anterior descending branch correlated with the anterior ischemic area score, and the sum of ST-segment deviations for the right coronary artery correlated with the inferior ischemic area score. The complex, but validated, formulas for anterior ischemic area and inferior ischemic area correlate well with the simpler sum of ST-segment deviations. Because the simpler sum is more clinically useful, it may provide an alternative for monitoring ischemic burden.

Residual area at risk after anterior myocardial infarction: Are ST segment changes during coronary angioplasty a reliable indicator? A comparison with technetium 99m-labeled sestamibi single-photon emission computed tomography

Background. The aim of this study was to assess whether, after anterior myocardial infarction, ST segment changes during percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending coronary artery correlated with the amount of ischemic myocardium in the area at risk, measured with 99mTc-labeled sestamibi single-photon emission computed tomography (SPECT) during balloon inflation. Methods and Results. Quantitative continuous monitoring of the ST segment was performed during PTCA of the left anterior descending coronary artery in 11 patients, and corresponding SPECT imaging was compared with a rest acquisition performed before PTCA. SPECT was quantified by a bull's-eye analysis according to main criteria: (1) the planimetered defect size during PTCA as an indicator of the size of the area at risk, (2) the change in the pathologic/normal area count ratio in the area at risk as an index of the severity of ischemia, and (3) the difference between the size of the defect during PTCA and at baseline. ST segment changes were correlated to the variation in pathologic/normal area count ratio (19% ± 14%; r = 0.61; p < 0.05) but not to the sizes of the scintigraphic defects. Conclusion. ST segment changes induced by occlusion of the infarct-related coronary artery during PTCA are related mostly to the severity of ischemia rather than to the size of the area at risk.

Silent ischemia after coronary angioplasty: Evaluation of restenosis and extent of ischemia in asymptomatic patients by tomographic thallium-201 exercise imaging and comparison with symptomatic patients

One hundred sixteen patients were evaluated to determine the ability of single photon emission computed tomographic (SPECT) thallium-201 exercise and redistribution imaging to detect silent ischemia secondary to restenosis in asymptomatic patients after single and multiple vessel percutaneous transluminal coronary angioplasty and the findings were compared with SPECT imaging detection of restenosis in symptomatic patients. The value of exercise electrocardiography (ECG) and the amount of ischemic myocardium in symptomatic and asymptomatic patients were determined. Forty-one patients were asymptomatic after angioplasty; 77% of these had chest pain before angioplasty. Seventy-five patients had chest pain after angioplasty; 99% of these had chest pain before angioplasty. Restenosis occurred in 61% of asymptomatic and 59% of symptomatic patients and in 46% of the vessels in both asymptomatic and symptomatic patients. Sensitivity, specificity and accuracy for detection of restenosis by SPECT in individual patients were 96%, 75% and 88% versus 91%, 77% and 85%, respectively, in the asymptomatic versus symptomatic groups (p = NS). Sensitivity, specificity and accuracy for restenosis detection in individual vessels were 90%, 89% and 89% versus 84%, 77% and 84%, respectively, in the asymptomatic and symptomatic groups (p = NS), with similar results for the three major arteries. Sensitivity and accuracy of exercise ECG were significantly less than those of SPECT imaging for the patients with silent (40% and 44%) and symptomatic (59% and 64%) ischemia (p less than 0.001). Restenosis of vessels in the patients with silent and symptomatic ischemia was associated with an equal amount and degree of severity of ischemic myocardium in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Factors that determine the occurrence of arrhythmias during acute myocardial ischemia

To elucidate the determinants of arrhythmias during acute myocardial ischemia, a 25-minute coronary artery occlusion was performed in 101 open-chest dogs. Heart rate correlated positively with the number of premature ventricular complexes (PVCs) and the occurrence of ventricular tachycardia (VT) and fibrillation (VF). The size of the occluded coronary bed was positively correlated with the occurrence of VF, but exhibited only a weak association with PVCs and VT. Coronary collateral flow exhibited a strong negative correlation with all forms of arrhythmias. Importantly, a sensitive coupling was present, whereby small differences in flow were associated with large differences in rhythm disorders. VT occurred in all ranges of occluded bed size examined, but within any given range, its incidence was inversely related to collateral flow. Thus, VT is relatively independent of occluded bed size, and is determined primarily by the degree of myocardial hypoperfusion. In contrast, even in the presence of low flows, VF did not develop with occluded beds <28% of left ventricular mass; above this critical occluded bed size, the incidence of VF was inversely related to collateral perfusion. VF is therefore determined by the association of a large occluded bed with a poor collateral function. This study identifies and systematically analyzes three major determinants of arrhythmias during acute myocardial ischemia: the heart rate, the amount of ischemic myocardium, and the severify of myocardial flow reduction. The finding that these factors account for most of the variability in the occurrence of malignant tachyarrhythmias has important methodological and clinical implications.