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Aim:This clinical practice guideline for the evaluation and diagnosis of chest pain provides recommendations and algorithms for clinicians to assess and diagnose chest pain in adult patients.Methods:A comprehensive literature search was conducted from November 11, 2017, to May 1, 2020, encompassing randomized and nonrandomized trials, observational studies, registries, reviews, and other evidence conducted on human subjects that were published in English from PubMed, EMBASE, the Cochrane Collaboration, Agency for Healthcare Research and Quality reports, and other relevant databases. Additional relevant studies, published through April 2021, were also considered.Structure:Chest pain is a frequent cause for emergency department visits in the United States. The “2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain” provides recommendations based on contemporary evidence on the assessment and evaluation of chest pain. This guideline presents an evidence-based approach to risk stratification and the diagnostic workup for the evaluation of chest pain. Cost-value considerations in diagnostic testing have been incorporated, and shared decision-making with patients is recommended.

Introduction: Despite the initial recovery from the acute COVID-19 infection, an increasing number of patients are experiencing a wide spectrum of symptoms more than 12 weeks after the index diagnosis. The underlying pathophysiology of post-acute sequelae of SARS-CoV-2 (PASC) syndrome remains unknown. Cardiovascular magnetic resonance (CMR) provides insight into pathophysiological mechanisms underlying cardiovascular disease. The relative concentration of phosphocreatine to ATP (PCr/ATP) measured non-invasively by 31-phosphorus magnetic resonance spectroscopy (31P-MRS) is a sensitive index of the myocardial energetic state. It is currently unknown whether PASC is associated with abnormalities of myocardial structure, function, perfusion and tissue characteristics or energetic derangement. Methods: A total of 13 patients with a clinical diagnosis of PASC syndrome (seropositive) and no prior underlying cardiovascular disease (CVD) and ten matching controls underwent 31P-MRS and CMR at 3T at a single time point. Results: Clinical characteristics and imaging results are provided in Table-1. Between the PASC syndrome patients and controls there were no differences in myocardial energetics (PCr/ATP), in cardiac structure (left ventricular volumes, mass), function (ejection fraction, global longitudinal strain), tissue characterization (T1 and extracellular volume fraction mapping, late gadolinium enhancement) or perfusion (myocardial rest and stress blood flow, myocardial perfusion reserve). Conclusion: Patients with a clinical PASC syndrome with no prior CVD exhibit no significant abnormalities in cardiac energetics, structure, function, myocardial blood flow or tissue characteristics.

Background— Surgery for severe mitral regurgitation is indicated if symptoms or left ventricular dilation or dysfunction occur. However, prognosis is already reduced by this stage, and earlier surgery on asymptomatic patients has been advocated if valve repair is likely, but identifying suitable patients for early surgery is difficult. Quantifying the regurgitation may help, but evidence for its link with outcome is limited. Cardiovascular magnetic resonance (CMR) can accurately quantify mitral regurgitation, and we examined whether this was associated with the future need for surgery. Methods and Results— One hundred nine asymptomatic patients with echocardiographic moderate or severe mitral regurgitation had baseline CMR scans and were followed up for up to 8 years (mean, 2.5±1.9 years). CMR quantification accurately identified patients who progressed to symptoms or other indications for surgery: 91% of subjects with regurgitant volume ≤55 mL survived to 5 years without surgery compared with only 21% with regurgitant volume >55 mL ( P 40%. CMR-derived end-diastolic volume index showed a weaker association with outcome (proportions surviving without surgery at 5 years, 90% for left ventricular end-diastolic volume index 2 versus 48% for ≥100 mL/m 2 ) and added little to the discriminatory power of regurgitant fraction/volume alone. Conclusions— CMR quantification of mitral regurgitation was associated with the development of symptoms or other indications for surgery and showed better discriminatory ability than the reference-standard CMR-derived ventricular volumes. CMR may be able to identify appropriate patients for early surgery, with the potential to change clinical practice, although the clinical benefits of early surgery require confirmation in a clinical trial.

Background— Coronary artery disease is the leading cause of death in women, and underdiagnosis contributes to the high mortality. This study compared the sex-specific diagnostic performance of cardiovascular magnetic resonance (CMR) and single-photon emission computed tomography (SPECT). Methods and Results— A total of 235 women and 393 men with suspected angina underwent CMR, SPECT, and x-ray angiography as part of the Clinical Evaluation of Magnetic Resonance Imaging in Coronary Heart Disease (CE-MARC) study. CMR comprised adenosine stress/rest perfusion, cine imaging, late gadolinium enhancement, and magnetic resonance coronary angiography. Gated adenosine stress/rest SPECT was performed with 99m Tc-tetrofosmin. For CMR, the sensitivity in women and men was similar (88.7% versus 85.6%; P =0.57), as was the specificity (83.5% versus 82.8%; P =0.86). For SPECT, the sensitivity was significantly worse in women than in men (50.9% versus 70.8%; P =0.007), but the specificities were similar (84.1% versus 81.3%; P =0.48). The sensitivity in both the female and male groups was significantly higher with CMR than SPECT ( P P =0.77 and P =1.00, respectively). For perfusion-only components, CMR outperformed SPECT in women (area under the curve, 0.90 versus 0.67; P P P =1.00) but was significantly worse in women with SPECT ( P Conclusions— In both sexes, CMR has greater sensitivity than SPECT. Unlike SPECT, there are no significant sex differences in the diagnostic performance of CMR. These findings, plus an absence of ionizing radiation exposure, mean that CMR should be more widely adopted in women with suspected coronary artery disease. Clinical Trial Registration— URL: http://www.controlled-trials.com . Unique identifier: ISRCTN77246133.

Background— Current indications for surgery in patients with significant aortic regurgitation (AR) focus on symptoms and left ventricular dilation/dysfunction. However, prognosis is already reduced by this stage, and earlier identification of patients for surgery could be beneficial. Quantifying the regurgitation may help, but there are limited data on its link with outcome. Cardiovascular magnetic resonance (CMR) can accurately quantify AR, and we examined whether this was associated with the future need for surgery. Methods and Results— One hundred thirteen patients with echocardiographic moderate or severe AR were monitored for up to 9 years (mean 2.6±2.1 years) following a CMR scan, and the progression to symptoms or other indications for surgery was monitored. AR quantification identified outcome with high accuracy: 85% of the 39 subjects with regurgitant fraction >33% progressed to surgery (mostly within 3 years) in comparison with 8% of 74 subjects with regurgitant fraction ≤33% ( P P 246 mL had good, although lower, discriminatory ability (area under the curve 0.88), but the combination of this measure with regurgitant fraction provided the best discriminatory power. Conclusions— High degrees of CMR-quantified AR were associated with the development of symptoms or other indications for surgery. Quantifying AR showed slightly better discriminatory ability than “gold standard” CMR ventricular volume assessment. This could provide a new paradigm for the timing of surgical intervention but requires confirmation in a clinical trial.

Introduction: Cardiovascular disease is the most common cause of premature mortality in rheumatoid arthritis (RA) & CV abnormalities are frequent in established disease. No studies have studied CV changes in treatment naive early RA (ERA). Hypothesis: Subclinical CV pathology exists in ERA as assessed by cardiovascular magnetic resonance (CMR). Methods: 66 ERA patients underwent 3T CMR scan including 355 modified Look-Locker inversion T1 maps before & 15 minutes after contrast administration. Patients had: no current/previous RA therapy; symptom duration Results: Patients & controls were well matched: the demographics & RA characteristics are in table 1. CMR measures are in table 2. Left ventricular (LV) mass & remodelling was significantly lower in ERA. There was no difference in LV volume or ejection fraction. Significantly lower aortic distensibility, a measure of increased arterial stiffness & CV risk, was found in ERA. Diffuse myocardial fibrosis, also associated with poorer outcomes & measured by extra-cellular volume, was increased significantly in ERA. Increased amount of non-ischaemic focal scarring was present in ERA but not significantly different compared to controls. Conclusions: This is the first CMR study of treatment-naive ERA. This well defined cohort demonstrates abnormalities in vascular function, myocardial tissue composition & LV geometry. This highlights presence of CV risk at the earliest stages of RA. Further investigation will determine the natural history including which effective therapy can modulate these abnormalities.

Many of the issues raised by Dr Einstein have been addressed in the article1 and in previous correspondence relating to the Clinical Evaluation of Magnetic Resonance Imaging in Coronary Heart Disease (CE-MARC) study.2,3 Einstein argues that the inclusion of magnetic resonance angiography offered cardiovascular magnetic resonance (CMR) an unfair advantage. However, as discussed in the article, secondary analyses from CE-MARC showed that excluding the magnetic resonance angiography component not only had a neutral effect on overall diagnostic accuracy, but actually led to a superior positive-predictive value for CMR in comparison with single-photon emission computed tomography (SPECT; owing to a reduction in false positives).2 We also included a detailed perfusion-only component analysis that Einstein makes no reference to in his critique. For perfusion-only components, CMR still significantly outperformed SPECT in females (area under the curve, 0.90 versus …

Background Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE). It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low. The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women. Methods and Results Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in NP (38±6.6 impulses/100 beats) was greater ( P P Conclusions Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group. The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.

An asymptomatic 26-year-old man was under routine surveillance following a Ross procedure at 17 years of age for bicuspid aortic valve disease. During transthoracic echocardiography there was a suspicion of homograft stenosis following the finding of a high-velocity turbulent jet in the main pulmonary artery (MPA) (Figure 1A and 1B; online-only Data Supplement Movie IA and IB). The pressure gradient by ultrasound Doppler was calculated to be 60 mm Hg, but the cause could not be clearly elucidated. The ECG (Figure 2) showed sinus rhythm with a normal axis, normal P-wave morphology, and nonspecific interventricular conduction delay in V1-V2. Chest radiograph (Figure 3) did not reveal any distortion of the great vessels or show signs of heart failure. Figure 1. A , Transthoracic echocardiography (parasternal-right ventricular outflow tract view) showing compression (horizontal arrow) of the main pulmonary artery. B , Color Doppler shows increased velocity in the main pulmonary artery (vertical arrow), but the study could not identify a clear cause. Figure 2. Standard 12-lead ECG. Figure 3. Chest radiograph (posteroanterior projection) showing a normal cardiothoracic ratio with no evidence of distortion of the pulmonary arteries or proximal aorta. A cardiovascular magnetic resonance (CMR) scan was organized to clarify the echocardiographic findings. CMR was …

We thank Dr Schlaich and colleagues for their letter finding that our publication1 has provided further information about the relationship between sympathetic activity and left ventricular hypertrophy, and particularly that it raises the need for future studies involving cardiac sympathetic activity. Their letter also raises concerns about the potential confounding effect of blood pressure (BP) and the heterogeneous nature of regional sympathetic output. We agree that ambulatory BP …

Background— Sympathetic activation has been implicated in the development of left ventricular hypertrophy (LVH). However, the relationship between sympathetic activation and LV mass (LVM) has not been clearly defined across a range of arterial pressure measurements. The present study was planned to determine that relationship, using cardiac magnetic resonance imaging to accurately quantify LVM, in hypertensive patients with and without LVH and in normal subjects. Methods and Results— Twenty-four patients with uncomplicated and untreated essential hypertension (LVH[−]) were compared with 25 patients with essential hypertension and left ventricular hypertrophy (LVH[+]) and 24 normal control subjects. Resting muscle sympathetic nerve activity was quantified as multiunit bursts and single units. Cardiac magnetic resonance imaging–determined LVM was indexed to body surface area (LVM index); in the LVH[−] group, LVM index was 67±2.1 g/m 2 , a value between those of the LVH[+] (91±3.4 g/m 2 ) and normal control (57±2.2 g/m 2 ) groups, respectively. The sympathetic activity in the LVH[−] group (53±1.3 bursts per 100 cardiac beats and 63±1.6 impulses per 100 cardiac beats) was between (at least P r =0.76, P Conclusions— These findings further support the hypothesis that central sympathetic activation is associated with the development of LVH in human hypertension.

Background —Reports demonstrating sympathetic hyperactivity in hypertension with the use of microneurography have been inconsistent. One possible reason is that previous studies have assessed muscle sympathetic nerve activity (MSNA) from integrated voltage waves (“bursts”) recorded from multiunit discharges. We studied single units with defined vasoconstrictor properties (s-MSNA) to further characterize sympathetic output in hypertensive disease. Methods and Results —We examined 74 subjects with a wide range of arterial blood pressure that were considered to be either normal (NT), high normal (HN), or stages 1 to 3 essential hypertension (EHT-1, EHT-2/3). All had their peripheral sympathetic activity measured from both multiunit bursts and single-unit vasoconstrictor impulses. There was a significant correlation between s-MSNA and MSNA, and results of variability studies were similar. The EHT-1 and EHT-2/3 groups had greater s-MSNA and MSNA than did the matched NT group (always P P P P Conclusions —Quantification from single vasoconstrictor units has provided additional evidence in established essential hypertension of increased central sympathetic output. Furthermore, in the mild or early stages of hypertension, this technique has provided new evidence of augmented sympathetic output compared with more severe hypertension.