Assessing myocardial perfusion after myocardial infarction.
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ABSTRACT:
SUBMITTER: Ashrafian H
PROVIDER: S-EPMC1420389 | biostudies-literature | 2006 Mar
REPOSITORIES: biostudies-literature
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Assessing myocardial perfusion after myocardial infarction.
Ashrafian Houman H Dwivedi Girish G Senior Roxy R
PLoS medicine 20060328 3
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Project description:Myocardial infarction with nonobstructive coronary arteries (MINOCA) has several possible underlying causes, including coronary microvascular dysfunction (CMD). Early cardiovascular magnetic resonance imaging (CMR) is recommended, however cannot provide a diagnosis in 25% of cases. Quantitative stress CMR perfusion mapping can identify CMD, however it is unknown if CMD is present during long-term follow-up of MINOCA patients. Therefore, this study aimed to evaluate presence of CMD during long-term follow-up in MINOCA patients with an initial normal CMR scan. MINOCA patients from the second Stockholm myocardial infarction with normal coronaries study (SMINC-2), with a normal CMR scan at median 3 days after hospitalization were investigated with comprehensive CMR including stress perfusion mapping a median of 5 years after the index event, together with age- and sex-matched volunteers without symptomatic ischemic heart disease. Cardiovascular risk factors, medication and symptoms of myocardial ischemia measured by the Seattle Angina Questionnaire 7 (SAQ-7), were registered. In total, 15 patients with MINOCA and an initial normal CMR scan (59 ± 7 years old, 60% female), and 15 age- and sex-matched volunteers, underwent CMR. Patients with MINOCA and an initial normal CMR scan had lower global stress perfusion compared to volunteers (2.83 ± 1.8 vs 3.53 ± 0.7 ml/min/g, p = 0.02). There were no differences in other CMR parameters, hemodynamic parameters, or cardiovascular risk factors, except for more frequent use of statins in the MINOCA patient group compared to volunteers. In conclusion, global stress perfusion is lower in MINOCA patients during follow-up, compared to age- and sex-matched volunteers, suggesting that CMD may be a possible pathophysiological mechanism in MINOCA.Clinical Trial Registration: Clinicaltrials.gov identifier NCT02318498. Registered 2014-12-17.
| S-EPMC10716406 | biostudies-literature
Project description:AIM: To appraise the efficacy of CD151-induced myocardial therapeutic angiogenesis in a pig myocardial infarction model. METHODS: CD151 and anti-CD151 were constructed into the recombinant adeno-associated virus (rAAV) vector. All 26 pigs were subjected to coronary artery ligation or no surgery. Eight weeks after coronary artery ligation, the expression of CD151 was measured by Western blot and immunostaining. Capillary density was evaluated using immunostaining for von Willebrand factor (vWF). 13N-labeled NH3 positron emission computed tomography ([13N]NH3PET) was measured to assess regional myocardial perfusion and the defect area. RESULTS: CD151 gene delivery could increase the expression of CD151 at protein level. Over-expression of CD151 increased the density of total capillaries in the ischemic myocardium, significantly improved the blood perfusion and reduced the defect area percentage. CONCLUSION: This study demonstrated that the rAAV-mediated CD151 gene delivery promoted efficient neovascularization and increased the blood perfusion after myocardial infarction in pigs.
| S-EPMC4006534 | biostudies-literature
Project description:BackgroundBoth stress cardiomyopathy (SCMP) and acute myocardial infarction (AMI) present with similar clinical symptoms and signs, and apical akinesis.HypothesisQuantitative segmental analysis of myocardial contrast echocardiography (MCE) helps to differentiate AMI from SCMP.MethodsReal-time MCE was performed in 33 consecutive patients who presented with an acute symptom/sign and a new apical akinesis on echocardiography. In 18 left ventricular (LV) myocardial segments, a replenishment curve was obtained in each segment to measure peak plateau myocardial contrast intensity (MCI) (A) and the replenishment curve slope (β). The calibrated MCI was also measured in each segment.ResultsAmong 33 patients, 22 were diagnosed with SCMP and 11 were diagnosed with AMI according to comprehensive diagnostic criteria. A, β, Aβ, and the calibrated MCI were lower in akinetic than in normokinetic segments in both the SCMP and AMI groups. In the akinetic segments, A, β, Aβ, and the calibrated MCI in SCMP patients were each higher than those in AMI patients. In patient-based analyses, areas under the ROC curves of A, β, Aβ, and the calibrated MCI for diagnosing AMI were 0.769, 0.607, 0.822, and 0.934, respectively. The optimal cutoff values to diagnose AMI were Aβ < 3.7 dB/sec (sensitivity 82%, specificity 82%) and a calibrated MCI < -23 dB (sensitivity 91%, specificity 95%).ConclusionsAlthough myocardial perfusion is relatively reduced in the akinetic segments of SCMP, a quantitative segmental analysis of myocardial perfusion using MCE helps to discriminate AMI from SCMP.
| S-EPMC6490539 | biostudies-literature
Project description:ObjectivesMacrophages play a central role in the cellular inflammatory response to myocardial infarction (MI) and predict subsequent clinical outcomes. We aimed to assess temporal changes in cellular inflammation and tissue oedema in patients with acute MI using ultrasmallsuperparamagnetic particles of iron oxide (USPIO)-enhanced MRI.MethodsThirty-one patients were recruited following acute MI and followed up for 3 months with repeated T2 and USPIO-enhanced T2*-mapping MRI. Regions of interest were categorised into infarct, peri-infarct and remote myocardial zones, and compared with control tissues.ResultsFollowing a single dose, USPIO enhancement was detected in the myocardium until 24 hours (p<0.0001). Histology confirmed colocalisation of iron and macrophages within the infarcted, but not the non-infarcted, myocardium. Following repeated doses, USPIO uptake in the infarct zone peaked at days 2-3, and greater USPIO uptake was detected in the infarct zone compared with remote myocardium until days 10-16 (p<0.05). In contrast, T2-defined myocardial oedema peaked at days 3-9 and remained increased in the infarct zone throughout the 3-month follow-up period (p<0.01).ConclusionMyocardial macrophage activity can be detected using USPIO-enhanced MRI in the first 2 weeks following acute MI. This observed pattern of cellular inflammation is distinct, and provides complementary information to the more prolonged myocardial oedema detectable using T2 mapping. This imaging technique holds promise as a non-invasive method of assessing and monitoring myocardial cellular inflammation with potential application to diagnosis, risk stratification and assessment of novel anti-inflammatory therapeutic interventions.Trial registration numberTrial registration number: 14663. Registered on UK Clinical Research Network (http://public.ukcrn.org.uk) and also ClinicalTrials.gov (https://clinicaltrials.gov/ct2/show/NCT02319278?term=DECIFER&rank=2).
| S-EPMC5629948 | biostudies-literature
Project description:BackgroundHyperglycaemia is known to result in oxidative stress tissue injury and dysfunction. Interestingly, studies have reported hepatic and renal oxidative stress injury during prediabetes; however, any injury to the myocardium during prediabetes has not been investigated. Hence this study aims to assess changes in the myocardial tissue in an HFHC diet-induced model of prediabetes.MethodsMale Sprague Dawley rats were randomly grouped into non-prediabetes and prediabetes (n = 6 in each group) and consumed a standard rat chow or fed a high-fat-high-carbohydrate diet respectively for a 20-week prediabetes induction period. Post induction, prediabetes was confirmed using the ADA criteria. Aldose reductase, NADH oxidase 1, superoxide dismutase, glutathione peroxide, cardiac troponins were analysed in cardiac tissue homogenate using specific ELISA kits. Lipid peroxidation was estimated by determining the concentration of malondialdehyde in the heart tissue homogenate according to the previously described protocol. Myocardial tissue sections were stained with H&E stain and analysed using Leica microsystem. All data were expressed as means ± SEM. Statistical comparisons were performed with Graph Pad instat Software using the Student's two-sided t-test. Pearson correlation coefficient was calculated to assess the association. Value of p < 0.05 was considered statistically significant.ResultsThe prediabetes group showed a markedly high oxidative stress as indicated by significantly increased NADH oxidase 1 and malondialdehyde while superoxide dismutase and glutathione peroxide were decreased compared to non-prediabetes group. There was no statistical difference between cardiac troponin I and T in the non-prediabetes and prediabetes groups. Cardiac troponins had a weak positive association with glycated haemoglobin.ConclusionThe findings of this study demonstrate that prediabetes is associated with myocardial injury through oxidative stress. Future studies are to investigate cardiac contractile function and include more cardiac biomarkers.
| S-EPMC9347129 | biostudies-literature
Project description:BackgroundMyocardial perfusion imaging (MPI) using single-photon emission computed tomography (SPECT) can in general be used safely in daily clinical practice. However, under the right circumstances, it can lead to serious complications.Case summaryA 68-year-old female patient with diabetes and a history of inferior ST-elevation myocardial infarction 8 years earlier, visited our outpatient clinic with atypical chest discomfort. In order to assess whether this is due to myocardial ischaemia, MPI-SPECT was ordered. As it was suspected she would not achieve sufficient exercise levels, pharmacologic stress using adenosine was arranged. During the scan, she developed acute myocardial infarction. Subsequent urgent coronary angiography demonstrated a subtotal stenosis in the proximal left anterior descending coronary artery which was successfully stented. She was still free from angina 4 months later.DiscussionThe combination of a reduced systemic and coronary perfusion pressure in the presence of an exhausted coronary autoregulation, may be a starting point for local geometrical changes that initiate the classic cascade of thrombus formation and acute occlusion of coronary arteries during MPI-SPECT. This illustrates the need for continuous patient and electrocardiogram monitoring.
| S-EPMC8086418 | biostudies-literature
Project description:IntroductionWe investigated if uptake pattern on myocardial perfusion SPECT (MPS) in patients with left bundle branch block (LBBB) is related to myocardial fibrosis, myocardial wall motion, and electrocardiography (ECG) characteristics.MethodsTwenty-three patients (9 women) with LBBB, examined with MPS and cardiac magnetic resonance (CMR), were included. Tracer uptake on MPS was classified by visual interpretation as typical LBBB pattern (Defect+, n = 13) or not (Defect-, n = 10) and quantitatively. CMR images were evaluated for wall thickness and for myocardial wall motion both by visual assessment and by regional myocardial radial strain from feature tracking, and for presence and location of myocardial fibrosis. ECGs were analyzed regarding QRS duration and the presence of strict criteria for LBBB.ResultsWall thickness was slightly lower in the septum compared to the lateral wall in Defect+ patients (5.6 ± 1.1 vs 6.0 ± 1.3 mm, P = 0.03) but not in Defect- patients (5.6 ± 1.0 vs 5.6 ± 0.9 mm, P = 0.84). Defect+ patients showed a larger proportion of dyskinetic segments in the septum and hyperkinetic segments in the lateral wall compared to Defect- patients (P = 0.006 and P = 0.004, respectively). Decreased myocardial radial strain was associated with decreased tracer uptake by MPS (R = 0.37, P < 0.001). Areas of fibrosis did not match areas with uptake defect on MPS. No differences in ECG variables were seen.ConclusionThe heterogeneous regional tracer uptake in some patients with LBBB is related to underlying regional myocardial dyskinesia, wall thickening, and wall thickness rather than stress-induced ischemia, myocardial fibrosis, or specific ECG characteristics.
| S-EPMC8709823 | biostudies-literature
Project description:BackgroundLeft ventricular (LV) remodeling has adverse effects on the prognosis of patients with myocardial infarction (MI). The aim of this study is to identify the risk factors of LV remodeling in MI patients by radionuclide myocardial imaging.Methods and resultsThis retrospective study consisted of 92 patients who had a history of definite prior MI on ECG and underwent both resting gated single photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) and positron emission tomography (PET) myocardial metabolism imaging. LV remodeling was defined as > mean + 2SD of LV end-diastolic volume index (LVEDVi) in the normal database. LV enlargement, cardiac dysfunction, wall thickening abnormalities expressed as summed thickening score (STS) were more severe in the old MI patients as compared to those with subacute MI. STS (Odds ratio, 1.296; P = .004) and the proportion of segments with reduced wall thickening in segments with normal perfusion (Odds ratio, 1.110; P = .001) were identified as the independent factors of LV remodeling in subacute and old MI patients in the multivariate binary regression model. Total perfusion deficit (TPD), viable myocardium, scar, and the proportion of segments with reduced wall thickening in segments with decreased perfusion showed strong correlation with LV remodeling in the univariate regression model as well.ConclusionsLV remodeling in old MI patients is more extensive and severe than that in subacute MI patients. LV wall thickening abnormalities as expressed by STS and the proportion of segments with reduced wall thickening in segments with normal perfusion are the independent risk factors of LV remodeling in MI patients.
| S-EPMC10958523 | biostudies-literature
Project description:BackgroundPreclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.Methods and resultsOverall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI.ConclusionsThe presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.
| S-EPMC4599491 | biostudies-literature
Project description:BackgroundIt has recently been demonstrated that the application of high-energy ultrasound and microbubbles, in a technique known as sonothrombolysis, dissolves intravascular thrombi and increases the angiographic recanalization rate in patients with ST-segment-elevation myocardial infarction (STEMI).ObjectiveTo evaluate the effects of sonothrombolysis on left ventricular wall motion and myocardial perfusion in patients with STEMI, using real-time myocardial perfusion echocardiography (RTMPE).MethodsOne hundred patients with STEMI were randomized into the following 2 groups: therapy (50 patients treated with sonothrombolysis and primary coronary angioplasty) and control (50 patients treated with primary coronary angioplasty). The patients underwent RTMPE for analysis of left ventricular ejection fraction (LVEF), wall motion score index (WMSI), and number of segments with myocardial perfusion defects 72 hours after STEMI and at 6 months of follow-up. P < 0.05 was considered statistically significant.ResultsPatients treated with sonothrombolysis had higher LVEF than the control group at 72 hours (50% ± 10% versus 44% ± 10%; p = 0.006), and this difference was maintained at 6 months of follow-up (53% ± 10% versus 48% ± 12%; p = 0.008). The WMSI was similar in the therapy and control groups at 72 hours (1.62 ± 0.39 versus 1.75 ± 0.40; p = 0.09), but it was lower in the therapy group at 6 months (1.46 ± 0.36 versus 1.64 ± 0.44; p = 0.02). The number of segments with perfusion defects on RTMPE was similar in therapy and control group at 72 hours (5.92 ± 3.47 versus 6.94 ± 3.39; p = 0.15), but it was lower in the therapy group at 6 months (4.64 ± 3.31 versus 6.57 ± 4.29; p = 0.01).ConclusionSonothrombolysis in patients with STEMI resulted in improved wall motion and ventricular perfusion scores over time.
| S-EPMC9007009 | biostudies-literature