Endogenous assessment of chronic myocardial infarction with T1ρ-mapping in patients

Background

Detection of cardiac fibrosis based on endogenous magnetic resonance (MR) characteristics of the myocardium would yield a measurement that can provide quantitative information, is independent of contrast agent concentration, renal function and timing. In ex vivo myocardial infarction (MI) tissue, it has been shown that a significantly higher T_1ρ is found in the MI region, and studies in animal models of chronic MI showed the first in vivo evidence for the ability to detect myocardial fibrosis with native T_1ρ-mapping. In this study we aimed to translate and validate T_1ρ-mapping for endogenous detection of chronic MI in patients.

Methods

We first performed a study in a porcine animal model of chronic MI to validate the implementation of T_1ρ-mapping on a clinical cardiovascular MR scanner and studied the correlation with histology. Subsequently a clinical protocol was developed, to assess the feasibility of scar tissue detection with native T_1ρ-mapping in patients (n = 21) with chronic MI, and correlated with gold standard late gadolinium enhancement (LGE) CMR. Four T_1ρ-weighted images were acquired using a spin-lock preparation pulse with varying duration (0, 13, 27, 45 ms) and an amplitude of 750 Hz, and a T_1ρ-map was calculated. The resulting T_1ρ-maps and LGE images were scored qualitatively for the presence and extent of myocardial scarring using the 17-segment AHA model.

Results

In the animal model (n = 9) a significantly higher T_1ρ relaxation time was found in the infarct region (61 ± 11 ms), compared to healthy remote myocardium (36 ± 4 ms) . In patients a higher T_1ρ relaxation time (79 ± 11 ms) was found in the infarct region than in remote myocardium (54 ± 6 ms). Overlap in the scoring of scar tissue on LGE images and T_1ρ-maps was 74%.

Conclusion

We have shown the feasibility of native T_1ρ-mapping for detection of infarct area in patients with a chronic myocardial infarction. In the near future, improvements on the T_1ρ -mapping sequence could provide a higher sensitivity and specificity. This endogenous method could be an alternative for LGE imaging, and provide additional quantitative information on myocardial tissue characteristics.     

Mapping myocardial viability using interleaved T 1—T 2 * weighted imaging

The present study was to evaluate the efficacy of our interleaved T1-T2* weighted imaging for assessing myocardial viability. The left anterior descending coronary artery (LAD) of pig hearts (n = 7) were occluded for 2 h, followed by 1 h reperfusion. After removed from animals, the hearts were perfused in a Langendorff apparatus with a mixture of pig blood and crystalloid solution in 1:1 ratio. T1 relaxation times of the myocardium were measured with a TurboFLASH inversion-recovery sequence. Gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) (0.05 mmol/kg body wt) was then injected as a bolus into the aortic perfusion line. The first pass of the contrast agent through the heart was followed using the interleaved T1-T2* imaging sequence. Once the concentration of the contrast agent was in an equilibrium state, T1 relaxation times were measured again. It was found that the percentage recovery of T2* intensity (PRT2*) at the maximum T1 intensity measured during the first pass of the contrast agent with the interleaved T1-T2* imaging was significantly higher in infarcted myocardium than in normal myocardium. Moreover, the regions showing a high T2* percentage recovery on PRT2* maps matched well with the infarcted myocardium demarcated with triphenyl tetrazolium chloride (TTC) staining. We therefore conclude that infarcted myocardium can be delineated using the interleaved T1-T2* imaging method.     

Review of myocardial bridge and its clinical significance

Myocardial bridge is a congenital anomaly of the coronary artery and appears on an angiogram as a systolic narrowing. Major coronary veins are rarely covered by myocardial bridges. The functional significance of the coronary bridge remains controversial. We reviewed the articles on this topic in recent years.DefinitionMyocardial bridging describes an angiographic entity,which is any degree of systolic narrowing of a coronary artery observed in at least one angiographic projection1. The main coronary arteries and the proximal segments of their major branches lie free on the epicardial surface of the heart. However, in some instances these vessels may penetrate into the muscle being surrounded by the myocardium, with the overlying muscle referred to as a "bridge". Myocardial bridging appears to be a congenital anomaly, due to failure of exteriorization of the primitive coronary intratrabecular arterial network2.     

Relation between myocardial edema and myocardial mass during the acute and convalescent phase of myocarditis – a CMR study

Background

Myocardial edema is a substantial feature of the inflammatory response in human myocarditis. The relation between myocardial edema and myocardial mass in the course of healing myocarditis has not been systematically investigated. We hypothesised that the resolution of myocardial edema as visualised by T2-weighted cardiovascular magnetic resonance (CMR) is associated with a decrease of myocardial mass in steady state free precession (SSFP)-cine imaging.

Methods

21 patients with acute myocarditis underwent CMR shortly after onset of symptoms and 1 year later. For visualization of edema, a T2-weighted breath-hold black-blood triple-inversion fast spin echo technique was applied and the ratio of signal intensity of myocardium/skeletal muscle was assessed. Left ventricular (LV) mass, volumes and function were quantified from biplane cine steady state free precession images.11 healthy volunteers served as a control group for interstudy reproducibility of LV mass.

Results

In patients with myocarditis, a significant decrease in LV mass was observed during follow-up compared to the acute phase (156.7 ± 30.6 g vs. 140.3 ± 28.3 g, p < 0.0001). The reduction of LV mass paralleled the normalization of initially increased myocardial signal intensity on T2-weighted images (2.4 ± 0.4 vs. 1.68 ± 0.3, p < 0.0001).In controls, the interstudy difference of LV mass was lower than in patients (5.1 ± 2.9 g vs. 16.3 ± 14.2 g, p = 0.02) resulting in a lower coefficient of variability (2.1 vs 8.9%, p = 0.04).

Conclusion

Reversible abnormalities in T2-weighted CMR are paralleled by a transient increase in left ventricular mass during the course of myocarditis. Myocardial edema may be a common pathway explaining these findings.     

Risk of myocardial infarction with non-steroidal anti-inflammatory drugs北大核心CSCD

BACKGROUND AND OBJECTIVE Inflammatory spondyloarthritis (SPA)has been associated with an increased risk of myocardial infarction (MI).Additionally,non-steroidal anti-inflammatory drugs (NSAIDs)have been associated with an increased risk of cardiovascular events.This study examined the effect of NSAIDs use on the risk of MI in patients with inflammatory arthritis or osteoarthritis (OA).     

Administration of atropine in the setting of acute myocardial infarction: potentiation of the ischemic process?

Atropine has also been suggested to potentially worsen the ischemic situation in patients who are in the midst of acute coronary ischemia. We report the case of a female patient with ischemic chest pain and third degree atrioventricular block who developed acute myocardial infarction (AMI) immediately after atropine administration. The use of atropine in this instance remains a reasonable option and should be strongly considered-despite this apparent complication. Undoubtedly in some cases, acute ischemia is intensified by hypoperfusion attributable to vagally mediated bradyarrhythmia; atropine is the antidote for such situations. An awareness of this potential adverse reaction coupled with a prudent selection of candidates for atropine therapy will show the risk/benefit ratio in each individual patient and, therefore, guide the clinician.     

Short-term prognosis of contemporary interventional therapy of ST-elevation myocardial infarction: does gender matter?

Background  

A higher mortality risk for women with acute ST-elevation myocardial infarction (STEMI) has been a common finding in the past, even after acute percutaneous coronary intervention (PCI). We set out to analyze whether there are gender differences in real-world contemporary treatment and outcomes of STEMI.     

Effect of Puerarin infection on impr oving motor tolerance of patients with acute myocardial infarction

Afteracutemyocardialinfarction（AMI），leftventricularchangescausedbychangesofleftventricularpumpfunctionandremodelingareimportantinfluencefactorstoearlyrecoveryofacutemyocardialinfarction．Thisarticlecomparedandobservedthetherapeuticeffectofpuerarininfectionon１２６casesofAMIandnormaltreatmentsandevaluatedthemthroughechocardiogramandwalkingtestofsixminutes．Nowreportsasfollowing：１Subjectandmethod１．１SubjectWeselected１２６in－patientswithAMIwhowererecruitedfrom１９９９～２０００．Dia…     

Subclinical myocardial inflammation and diffuse fibrosis are common in systemic sclerosis – a clinical study using myocardial T1-mapping and extracellular volume quantification

Background

Systemic sclerosis (SSc) is characterised by multi-organ tissue fibrosis including the myocardium. Diffuse myocardial fibrosis can be detected non-invasively by T1 and extracellular volume (ECV) quantification, while focal myocardial inflammation and fibrosis may be detected by T2-weighted and late gadolinium enhancement (LGE), respectively, using cardiovascular magnetic resonance (CMR). We hypothesised that multiparametric CMR can detect subclinical myocardial involvement in patients with SSc.

Methods

19 SSc patients (18 female, mean age 55 ± 10 years) and 20 controls (19 female, mean age 56 ± 8 years) without overt cardiovascular disease underwent CMR at 1.5T, including cine, tagging, T1-mapping, T2-weighted, LGE imaging and ECV quantification.

Results

Focal fibrosis on LGE was found in 10 SSc patients (53%) but none of controls. SSc patients also had areas of myocardial oedema on T2-weighted imaging (median 13 vs. 0% in controls). SSc patients had significantly higher native myocardial T1 values (1007 ± 29 vs. 958 ± 20 ms, p < 0.001), larger areas of myocardial involvement by native T1 >990 ms (median 52 vs. 3% in controls) and expansion of ECV (35.4 ± 4.8 vs. 27.6 ± 2.5%, p < 0.001), likely representing a combination of low-grade inflammation and diffuse myocardial fibrosis. Regardless of any regional fibrosis, native T1 and ECV were significantly elevated in SSc and correlated with disease activity and severity. Although biventricular size and global function were preserved, there was impairment in the peak systolic circumferential strain (-16.8 ± 1.6 vs. -18.6 ± 1.0, p < 0.001) and peak diastolic strain rate (83 ± 26 vs. 114 ± 16 s-1, p < 0.001) in SSc, which inversely correlated with diffuse myocardial fibrosis indices.

Conclusions

Cardiac involvement is common in SSc even in the absence of cardiac symptoms, and includes chronic myocardial inflammation as well as focal and diffuse myocardial fibrosis. Myocardial abnormalities detected on CMR were associated with impaired strain parameters, as well as disease activity and severity in SSc patients. CMR may be useful in future in the study of treatments aimed at preventing or reducing adverse myocardial processes in SSc.