Diagnostic accuracy of Left atrial function and strain for differentiating between acute and chronic myocardial infarction

doi:10.21203/rs.3.rs-2116652/v1

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Research Article

Diagnostic accuracy of Left atrial function and strain for differentiating between acute and chronic myocardial infarction

https://doi.org/10.21203/rs.3.rs-2116652/v1

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Journal Publication

published 28 Apr, 2023

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Background

The left atrial strain and strain rate in patients with myocardial infarction (MI) were measured using the cardiac magnetic resonance tissue tracking (CMR-TT) technique, and its usefulness in the quantitative assessment of myocardial infarction for differentiating between acute and chronic myocardial infarction was assessed.

Methods

Consecutive 36 AMI patients and 29 CMI patients who underwent CMR were retrospectively analyzed as well as 30 controls. By analyzing the strain from long and short left ventricular view cines from CMR-TT, the left atrial and ventricular functions were measured. Receiver operating characteristic(ROC) analysis was used to test the diagnostic accuracy of the CMR-TT strain parameters in distinguishing acute from chronic myocardial infarction.

Results

Participants in both AMI and CMI demonstrated decreased LA reservoir function, conduit function, and LA booster pump dysfunction as compared to the controls. The LA strain was more sensitive than the LV global strain for determining the stage of MI. Of all the LA strain parameters measured, SRa produced the best areas under the ROC curve (AUC) of 0.879 in demonstrating distinction between acute and chronic myocardial infarction. The LV strain and LA functional parameters showed the largest significant differences between chronic myocardial infarction and normal (P < 0.001, respectively), while there was no difference between AMI and normals.

Conclusions

CMR-TT-derived LA strain is a promising and robust tool for demonstrating impaired LA mechanics and quantifying LA dynamics, both of which have high sensitivity and specificity in the differential diagnosis of acute versus chronic myocardial infarction, and their use in clinical application is thus worth promoting.

Cardiac magnetic resonance (CMR)

acute myocardial infarction (AMI)

tissue tracking

chronic myocardial infarction (CMI)

left atrial strain

LVEF

strain

LGE

Left atrial function

Myocardial infarction (MI) is caused by a severe reduction or stoppage in blood flow to the myocardium, resulting in myocardial cell death and subsequent compensatory fibrosis as well as decreased systolic and diastolic function of the wounded myocardium^[1]. In turn, myocardial infarction is a significant global burden, accounting for the leading cause of mortality^[2]. The evaluation, treatment, and follow-up of AMI and CMI varies dramatically in clinical practice. Late gadolinium enhancement (LGE) is the gold standard for quantifying the extent and magnitude of a myocardial infarction^[3], however its use in distinguishing AMI from CMI is restricted.

In recent years, cardiovascular magnetic resonance tissue tracking (CMR-TT) has been widely used in clinical research and practice to assess myocardial deformation by monitoring tissue motion under steady-state free motion (SSFP).^[4]. CMR-TT can detect early distortion of the left ventricle and atrium without the use of contrast^[5]. It has a higher spatial resolution, a bigger field of view, and better consistency than speckle-tracking echocardiography (STE), and it can more accurately depict the functional features of cardiac tissue^[6]. CMR is a strong imaging tool that can offer a thorough depiction of MI, including LV remodeling and decreased function^[7]. The significance of left atrial (LA) function and structure has recently been acknowledged, and atrial cardiomyopathy has been considered as a distinct entity. During hemodynamic stress or exercise, the LA works as a reservoir, conduit, and booster pump, regulating left ventricular diastolic filling and cardiac performance^{[8, 9]}. Increased atrial volumes are frequently linked to cardiovascular illnesses such ischemic heart disease, valvular heart disease, and heart failure^[10]. However, strain and strain rate, in addition to LA volume following AMI, may be sensitive markers of left atrial function and have been used to predict death from cardiovascular illness^{[11, 12]}.

In this study, we aim to compare the LA and LV structural and functional parameters between patients and controls through CMR-TT, and to investigate the capability of LA function and strain in distinguishing AMI from CMI and providing clinical implications.

Study Participants

36 consecutive patients with AMI and 29 consecutive patients with CMI who underwent CMR at our hospital between January 2016 and December 2021 were retrospectively included in this study with comparable gender and age distribution.The inclusion criteria for AMI patients were as follows: (1)the patients had to experience an AMI for the first time with a recognized culprit coronary artery;(2)All patients underwent successful reperfusion with percutaneous coronary intervention. In line with the recommendations of the American College of Cardiology and the European Society of Cardiology^[13], AMI was identified by the patient's history, electrocardiographic alterations, cardiac biomarker abnormalities, and coronary angiography. The following criteria for CMI include: (1)significant chest pain lasting more than 30 minutes; (2)a history of MI that is certain and longer than 3 months; and (3)confirmation of coronary artery stenosis by digital subtraction angiography or computed tomography angiography testing. Severe claustrophobia, known cardiomyopathy, prior cardiac surgery, severe chronic kidney disease, an allergy to gadolinium, and ferrous iron implants were among the exclusion criteria. There were 29 healthy people who did not have any indications of cardiovascular illness and had normal electrocardiogram (ECG) results. The study protocol is performed in accordance with the relevant guidelines. Because it is a retrospective study, written informed consent was waived and the study received approval from our hospital committee.

Cardiac MRI Protocol

Study participants underwent cardiac MRI with clinical 1.5T scanners. With cardiac vector ECG and respiratory gating for scanning, we were able to get tissue characterization and function in two- and four-chamber long-axis views as well as short-axis pictures of the left ventricle. The scan parameters of cine images of Philips Achieva was follows: TR/TE = 3.38/1.69 ms, FOV: 69.8×32 cm; layer thickness 8 mm, layer interval 2 mm, matrix 192×180, and flip angle 60°. Gadopentetate glucosamine (Gd-DTPA) was used as the contrast agent, at a dose of 0.2 mmol/kg and an infusion rate of 2.0 ml/s. After the contrast agent was injected, 20 ml of saline was injected at the same rate, and delayed enhancement scans of the heart were done 15 minutes after the contrast agent was injected intravenously. The delayed enhancement scan parameters were TR/TE = 6.12/3.00 ms, layer thickness 8 mm, layer spacing 2 mm, matrix 152×200.

CMR analysis

All CMR analyses were completed offline with commercially accessible software (CVI42 version 5.12.4, Circle Cardiovascular Imaging, Calgary, Canada). By highlighting the endo- and epicardial boundary on LV short-axis cine images, parameters of left ventricular function were conducted (papillary muscles were excluded). The computer automatically tracks the endocardial and epicardial displacements to quantify the motion of the left ventricular myocardium. Following that, measurements of the left ventricle's end-diastolic volume (LVEDV), end-systolic volume (LVESV), ejection fraction (LVEF), cardiac output (CO), cardiac index (CI), and mass (LVM) were made. The left ventricle (LV) global peak strain (LV-GPSr), left ventricle global peak strain (LV-GPSc), and left ventricle global peak strain longitudinal (LV-GPSL) values were obtained by autonomously measuring the deformation of myocardial motion during the cardiac cycle (LV-GPSl). The gold standard for identifying infarcted segments was LGE. The infarct size was defined as the hyper-enhanced region with a signal intensity threshold ≥ 5 standard deviations (SD) above the distant myocardium's mean signal intensity.

LA function was measured by semi-automatically tracking the LA endocardial and epicardial borders in long-axis two- and four-chamber views at end-systole and end-diastole, excluding pulmonary veins and LA appendages. Maximum LA volumes were measured at the end-diastole(LAVmin) and end-systole(LAVmax), at ventricular diastole prior to atrial contraction (LAVpac) respectively. The following equation described left atrial fraction as fractional volume changes: total ejection fraction [LA total EF] = (LAVmax − LAVmin) × 100%/LAVmax, passive ejection fraction [LA passive EF]= (LAVmax − LAVpre-a) × 100%/LAVmax, active ejection fraction [LA active EF] = (LAVpre-a − LAVmin) × 100%/LAVpre-a. The strain and strain rate values for each tissue point were automatically derived by the software(Fig. 1), including total strain [εs], peak positive strain rate [SRs], passive strain [εe], peak early-negative SR [SRe], active strain [εa], peak late-negative SR [SRa].

Reproducibility

The intraclass correlation coefficient (ICC) was used to evaluate the intra- and inter-observer variability for the LA volume, strain, and strain rate measures in 20 randomly chosen participants (10 healthy subjects and 10 MI patients). By re-evaluating the same 20 participants after a month, the same observer was able to demonstrate intra-observer repeatability. Two researchers who were blind to each other's findings evaluated the inter-observer repeatability of their findings.

Statistical analysis

Statistical analyses were performed on SPSS version 26.0 (IBM, Armonk, NY, USA). Measured data were shown as mean ± SD. Categorical variables were expressed as numbers and percentages. Fisher's exact test or χ2 tests were used to compare categorical variables. The three groups were compared using one-way analysis of variance (ANOVA) followed by Tukey's or Games-Howell's post hoc paired comparison tests. Independent samples t-test was used to compare global LV strain and infarct volume in AMI and CMI. The Receiver Operating characteristic Curve (ROC) was used to analyze the value of lLA strain and strain rate parameters in the identification of AMI and CMI. Statistically significant differences were P values < 0.05.

Patient characteristics

81 patients were initially recruited and were excluded due to poor image quality (n = 11) and absence of LGE (n = 5). In the final study cohort, 36 patients with AMI and 29 patients with CMI were included in this study for analysis, along with size- and gender-matched controls. There were no significant differences among the three groups in terms of gender and body mass index. Baseline information is shown in Table 1.

Table 1

Baseline clinical characteristics
	AMI(n = 36)	CMI(n = 29)	Control(n = 30)	P value
Clinical baseline
Age, y	51.00 ± 2.70	61.78 ± 2.19	55.60 ± 2.78	0.087
Male, n(%)	30(83)	23(79)	23(77)	0.792
Height, cm	166.16 ± 1.89	165.06 ± 1.50	162.47 ± 2.54	0.317
Weight, kg	65.85 ± 2.49	65.64 ± 2.36	68.57 ± 4.06	0.880
BMI, (kg/m²)	23.90 ± 0.89	24.00 ± 0.71	25.80 ± 1.165	0.405
Diabetes, n(%)	13(36)	12(41)	-	0.664
Hypertension, n(%)	18(50)	14(48)	-	0.890
Hyperlipidemia, n(%)	5(14)	2(6.9)	-	0.447
Smoker, n(%)	30(83)	19(66)	-	0.097
Data are expressed as mean ± standard deviations or percentages in parentheses. There was no significant difference between MI and controls.

Left ventricular structural and functional abnormality

As shown in Table 2, In comparison to patients with AMI and the controls, patients with CMI had higher LV end-diastolic and end-systolic volumes, as well as a higher LV mass index; controls also had a higher LVEF. There was no discernible difference in LV SV, CO, or CI among these groups. Between AMI and CMI, there was no difference in Infarct volume or LV strain.(Fig. 2).

Table 2

LV function and strain parameters
	AMI(n = 36)	CMI(n = 29)	Control(n = 30)	P1 values	P2values	P3values
LV conventional parameters
LV EDV(ml)	134.95 ± 6.52	194.95 ± 13.42	124.92 ± 7.70	0.000	0.623	0.000
LV ESV(ml)	71.35 ± 6.79	121.12 ± 13.04	47.09 ± 1.89	0.001	0.154	0.000
LV SV(ml)	63.59 ± 4.16	73.82 ± 5.00	77.83 ± 7.67	0.339	0.287	0.975
LV EF(%)	48.36 ± 3.32	40.0 ± 3.40	60.81 ± 2.86	0.150	0.031	0.000
LV CO(l/min)	4.56 ± 0.27	5.23 ± 0.41	5.05 ± 0.45	0.371	0.759	0.852
CI(l/min/m2)	2.58 ± 0.15	2.96 ± 0.22	2.85 ± 0.23	0.329	0.703	0.861
LV Mass(g)	124.88 ± 6.35	159.23 ± 16.05	99.36 ± 5.79	0.044	0.135	0.000
Infarct volume (%LV)	15.80 ± 8.79	14.26 ± 5.38	-	0.696
LV strain
LV-GPSr (%)	20.03 ± 9.025	16.50 ± 9.66	-	0.284
LV-GPSc (%)	-14.84 ± 5.25	-11.99 ± 4.55	-	0.110
LV-GPSl (%)	-9.91 ± 4.19	-8.77 ± 3.64	-	0.417
P1 for AMI versus CMI. P2 for AMI versus normal controls. P3 for CMI values versus normal controls. Bold values indicate statistical significance. There was no difference between AMI and CMI about infarct volume and LV global peak strain.

Left atrial dysfunction

Table 3 compares LA volumes and functional indices in the three groups. pre-systolic LA volumes, maximal and minimal volumes were the greatest in CMI. LA total, passive and active EF showed significantly lower in CMI compared with AMI and controls (all P < 0.01). Left atrial strain and strain rate showed significant differences in these three groups (all P < 0.05), but there was no statistical difference in SRe between normal and AMI(p = 0.088) (Fig. 3, 4).

Table 3

LA volumetric and deformation parameters assessed by CMR-FT
	AMI(n = 36)	CMI(n = 29)	Control(n = 30)	P1values	P2values	P3values
LA volumetric parameters
Vmax, ml	33.95 ± 1.95	46.94 ± 3.0	39.45 ± 1.47	0.000	0.047	0.017
Vpre-a, ml	28.94 ± 1.69	42.36 ± 2.78	32.72 ± 1.32	0.000	0.376	0.003
Vmin, ml	22.17 ± 1.44	37.92 ± 2.69	25.28 ± 1.26	0.000	0.513	0.000
LA reservoir function
EF-total	34.70 ± 1.97	19.36 ± 1.99	36.36 ± 1.19	0.000	1.000	0.000
εs, %	24.18 ± 1.80	14.27 ± 2.03	34.63 ± 1.33	0.001	0.000	0.000
SRs, s-1	1.23 ± 0.089	0.75 ± 0.10	1.57 ± 0.10	0.005	0.029	0.000
LA conduit function
EF-passive	14.81 ± 1.41	9.70 ± 1.13	17.16 ± 0.67	0.011	0.359	0.000
εe, %	13.01 ± 1.38	6.47 ± 1.42	18.89 ± 1.07	0.004	0.003	< 0.0001
SRe, s-1	-1.37 ± 0.156	-0.64 ± 0.10	-1.80 ± 0.15	0.005	0.088	0.000
LA booster pump function
EF-active	23.49 ± 1.60	10.78 ± 1.57	23.22 ± 1.15	0.000	1.000	0.000
εa, %	11.17 ± 0.75	7.79 ± 0.98	15.73 ± 0.87	0.032	0.000	0.000
SRa, s-1	-1.52 ± 0.098	-0.85 ± 0.12	-1.98 ± 0.14	0.002	0.017	0.000
P1 for AMI versus CMI. P2 for AMI versus normal controls. P3 for CMI values versus normal controls. Bold values indicate statistical significance. There was significant difference among three groups about LA strain and strain rate.

Cardiac MR strain parameters for differentiating between AMI and CMI

Of all LA strain and strain rate parameters obtained, SRa produced the best AUC in distinguishing AMI from CMI, which was 0.879 (Fig. 5). Although left atrial function parameters (including volume and ejection fraction) can be used to discriminate between AMI and CMI, they are not statistically significant in normal and acute patients.

Reproducibility

The intra- and inter-observer level were observed in LA volumetric and deformation parameters. The CV% and ICC are summarized in Table 4.

Table 4

Reproducibility of the LA strain and function analysis by CMR-FT
	Intra-observer		Inter-observer
	ICC	95% CI	ICC	95% CI
εs, %	0.970	0.783–0.997	0.891	0.447–0.988
εe, %	0.962	0.882–0.988	0.837	0.560–0.947
εa, %	0.959	0.867–0.987	0.883	0.646–0.962
SRs, s-1	0.946	0.840–0.982	0.859	0.578–0.954
SRe, s-1	0.947	0.846–0.982	0.850	0.290–0.959
SRa, s-1	0.949	0.857–0.984	0.846	0.310–0.975
Vmax, ml	0.981	0.942–0.994	0.945	0.832–0.983
Vpac, ml	0.963	0.891–0.988	0.943	0.643–0.994
Vmin, ml	0.972	0.913–0.991	0.937	0.539–0.993
EFtotal, %	0.979	0.937–0.994	0.911	0.718–0.973
EFpassive	0.973	0.917–0.991	0.897	0.714–0.942
EFbooster	0.972	0.908–0.991	0.921	0.765–0.975
LA, left atrial; ICC = intraclass correlation coefficient; CI, confidence interval.

The current study assessed the diagnostic accuracy of LA function and strain parameters by CMR-TT in order to distinguish between AMI and CMI. Our findings demonstrate that the myocardial infarction stage of patients can be determined and tracked using quantitative tissue methods in a noncontrast manner. According to measurements, LA strain and strain rate are the main factors separating AMI from CMI. The results of our study lead to several important advances: (I) there were significant differences in the strain and strain rate parameters among AMI, CMI, and controls; these parameters could be utilized to track the staging of MI; (II) SRa of LA was the best at discriminating about AMI and CMI, with high diagnostic accuracy; (III) Patients with acute and chronic myocardial infarction can be recognized using left atrial function parameters, however there is no difference between the AMI and normals; (IV) The left global ventricular strain cannot be used to differentiate acute from chronic infarction; As a result, quantitative measurement of LA strain and strain rate could be a valuable tool for noninvasive evaluation, identification, and classification of acute and chronic infarction.

Left ventricular performance and LVEF are most commonly quantified to assess cardiac function in cardiovascular diseases^[14]. This study found that patients with CMI had bigger left ventricular systolic and end-diastolic volumes than patients with AMI and normal controls, although AMI was not significantly different from normal controls. It has been said that the reaction to an ischemia event is a dynamic process. Ventricle expansion is a defining characteristic of the subsequent LV remodelling. But this changes are frequently observed late in the course of the illness^[15–17]. The cardiac workload of the remaining viable myocardium is increased by non-viable infarcted tissue, which results in compensatory hypertrophy^{[18, 19]}. While maintaining blood flow to the systemic circulation through this compensatory mechanism may be seen as a good thing, it also causes higher systolic and diastolic wall stresses, which in turn cause decreased ejection fraction and ventricular dilatation in the later stages^{[20, 21]}. Even if the left ventricular ejection fraction is preserved, it is difficult to accurately reflect myocardial function^[22]. This study shown that the left ventricular ejection fraction was lower in patients with AMI and CMI than in controls, although there was no significant difference between AMI and CMI. This may be because myocardial ischemia necrosis and hypokinesis lower the left ventricular ejection fraction following myocardial infarction. Patients with chronic myocardial infarction tend to have a further decrease in ejection fraction as the illness progresses. The value of left ventricular ejection fraction is limited by reflecting only global left ventricular function.

Compared to LVEF, strain parameters is a metric that is more sensitive to cardiac function. The use of the TT approach has made it possible for CMR to perform trustworthy strain analyses, and prior research has in fact confirmed the reliability and validity of TT-CMR in a variety of patient populations^{[23, 24]}, including MI patients. Myocardial strain analysis has emerged as a more complete approach for assessing LV function, allowing for the measurement of global and regional myocardial deformation during the cardiac cycle^[25]. This study showed there was no statistically significant difference in left ventricular strain between AMI and CMI. Myocardial ischemia can cause myocardial distortion in the lesion section, the decline of myocardial function, and a reduction in exercise—these changes of the myocardium will give rise to LV or myocardial fibrosis developed, which making for lower myocardial motion and strain^[26]. That global strain are only an indicator of global heart function and cannot be used to differentiate the AMI and CMI. However, some studies^[27–29] have shown that local strain parameters can distinguish between acute and chronic infarction. The reason for this analysis is that the research^[29] was a longitudinal study. This study, on the other hand, was a cross-sectional study, although there was no difference in myocardial infarct area and left ventricular global strain between AMI and CMI, which implys LV globle strain has little significance for staging of MI. However, the local myocardial strain is influenced by a number of variables (such as local myocardial infarction degree, infarct area, presence of MVO, etc.), and its reproducibility is poor, so it was not examined in this study.

In the setting of mild diastolic dysfunction, preserved LA active function represents a compensatory mechanism for maintaining volume and LV filling, and its deterioration reflects the "decompensated" phase of reduced LA compliance^[30]. In this study, AMI patients had lower left atrial volume and ejection fraction than CMI, but they were not statistically different from the normals. After MI, the myofibroblasts gradually replace myocytes, which enhanced LV stiffness, influenced blood flow from the LA into the LV, and caused the LA to increase preload in a certain range^[31]. Within certain limits, LA contraction also follows the Frank-Starling mechanism, which implies the contractile work of LA depends on the volume of its active systolic preload. In light of this, LA deformation may be compensatorily enhanced within a certain range^[32]. In AMI patients, preserved LA ejection function provides a compensatory strategy for maintaining stroke volume and LV filling^[33]. CMI may lead to chronic LA myocardial hypoperfusion, which may further impair LA contractility or decrease LA compliance^[34]. The impaired LA function may not only be related to the reduced LV systolic and diastolic functionand but also precede left atrial enlargement and abnormal left ventricular longitudinal function^{[35, 36]}. Although left atrial function parameters (including volume and ejection fraction) can be used to distinguish between acute and chronic infarction, the above parameters are not statistically significant in normal and acute patients, making it impossible to determine whether values greater than the threshold are normal or acute infarction patients.

LA strain and strain rate were impaired in MI, and there were difference among three groups. In our cohort, despite the fact that there were no differences in LA volumetric metrics between AMI and controls, impaired LA strain are already impaired in AMI patients. This finding supported the concept that LA strain, derived of CMR, has diagnostic utility for the stage of MI. The area under the ROC curve demonstrates that strain and strain rate have higher diagnostic characteristics for identifying AMI and CMI. Left atrial strain is significantly impaired in both AMI and CMI. It is in agreement with Zhou D's^[37] study suggesting that LA deformation-related damage may manifest even sooner than the LV strain in the MI. This result demonstrated that in those individuals, LV strain was not the most reliable parameter for identifying early damage. Therefore, it is crucial to assess LA strain and strain rate in patients with AMI or CMI. Previous research shown that, before the clinically obvious LV functional disorders in AMI, LA strain might represent myocardial deformation^{[12, 38]}. LA strain decrease may signify a severe impairment of atrial compensatory ability^[39], which might account for its great prognostic value in some studies. This predictive usefulness has also been shown in hypertrophic cardiomyopathy, where inadequate LA reservoir strain markedly raised the probability of death and the onset or progression of HF^{[40, 41]}. In another study, LA dysfunction by TT was a separate predictor of HF development in the asymptomatic general population^[42]. Nayyar, D^[39] et al described that there was an increase in atrial booster pump activity that served as a compensatory mechanism after STEMI. Conduit function has a critical role in maintaining exercise capacity, according to data from the population of people with heart failure with intact ejection fraction^[43]. When the LV base descends during systole, the LA strain reflects atrial compliance and, to a lesser extent, atrial contractility and relaxation.^{[44, 45]}. It is clear that LA strain has a more clinical application. A possible explanation may be related to anatomy: the LA is a very thin wall that is extremely sensitive to the subtle stimuli^[46]. Therefore, as an early parameter, the strain of the LA may be more sensitive than LV when distinguishing AMI from CMI.

The main limitations of this study might be attributed to the participants' individual differences and the limited sample size. For the quantitative diagnosis between AMI and CMI made possible by this technique, more samples would still be required to establish the diagnostic threshold. Secondly, There is no classification of the duration of CMI, it's probable that the longer it lasts, the more prominent the alterations in left cardiac parameters will be.

CMR-TT-derived LA strain is a promising and robust tool for demonstrating impaired LA mechanics and quantifying LA dynamics, which have high sensitivity and specificity in the differential diagnosis of acute versus chronic myocardial infarction, and their use in clinical application is thus worth promoting.

CMR-TT-derived LA strain is a promising and powerful tool for demonstrating impaired LA mechanics and quantifying LA dynamics with high sensitivity and specificity in the differential diagnosis of AMI and CMI, making it worth promoting in clinical applications.

Acknowledgements

We appreciate the effort of the individuals to executing this study.

Author contributions

All authors made a significant contribution to this study. JXF and YY designed this study and collected the clinical data. JXF, YZ, LYT and WM analyzed the data. JXF and JJ drafted the manuscript. JJ, FB and YY supervised this study and revised the article.

Funding

This study has no funding.

Availability of data and materials

The data underlying this article will be shared on reasonable request to the corresponding author.

Ethics approval and consent to participate

The study was approved by The Fifth People's Hospital of Chengdu. Informed consent was waived due to the retrospective nature of the study.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no commercial interests.

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No competing interests reported.

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published 28 Apr, 2023

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Diagnostic accuracy of Left atrial function and strain for differentiating between acute and chronic myocardial infarction

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