Search Results (9)

Background: Myocardial fibrosis in aortic stenosis (AS) is associated with a significant risk of poor clinical outcomes. Myocardial fibrosis can be evaluated using cardiovascular magnetic resonance (CMR) imaging and may be useful for risk-stratifying patients at high risk for poorer outcomes. A circulating biomarker of fibrosis may be a cheaper, more accessible alternative to CMR in lower-to-middle-income countries. This study evaluated the correlation between serum biomarkers of myocardial fibrosis (TGF-β1, PICP, and PIIINP) with CMR markers of myocardial fibrosis (T1 mapping, extracellular volume fraction (ECV), and late gadolinium enhancement (LGE)). Methods: Twenty-one high-gradient (mean gradient ≥ 40 mmHg) severe AS (aortic valve area < 1.0 cm²) participants underwent T1 mapping and LGE imaging using CMR. Blood serum was collected for enzyme-linked immunosorbent assays of the listed biomarkers. Results: Serum TGF-β1 was associated significantly with the global T1 relaxation time on CMR (r = 0.46 with 95% CI 0.03 to 0.74, p = 0.04). In the high T1 time group (1056 vs. 1023 ms), trends toward elevated serum TGF-β1 concentration (13,044 vs. 10,341 pg/mL, p = 0.08) and ECV (26% vs. 24%, p = 0.07) were observed. The high T1 and trend towards elevated TGF-β1 concentration in this group tracked adverse LV remodeling and systolic dysfunction. There were no significant associations between PICP/PIIINP and T1 mapping or between the biomarkers and LGE quantity. Conclusions: Serum TGF-β1 is a potential surrogate for diffuse interstitial fibrosis measured by T1 mapping and ECV on CMR. Serum PICP and PIIINP may be less appropriate as surrogate markers of fibrosis in view of their temporal trends over the course of AS. Larger studies are needed to validate the utility of TGF-β1 as a marker of diffuse fibrosis and to evaluate the utility of serial PICP/PIIINP measurements to predict decompensation. Full article

Aortic stenosis (AS) is associated with the development of replacement myocardial fibrosis/scar. Given the dose-dependent relationship between scar and clinical outcomes after aortic valve replacement (AVR) surgery, scar quantity may serve as an important risk-stratification tool to aid decision-making on the optimal timing of AVR. Scar is non-invasively assessed and quantified by cardiovascular magnetic resonance (CMR) imaging. Several quantification techniques exist, and consensus on the optimal technique is lacking. These techniques range from a visual manual method to fully automated ones. This review describes the different scar quantification techniques used and highlights their strengths and shortfalls within the context of AS. The two most commonly used techniques in AS include the semi-automated signal threshold versus reference mean (STRM) and full-width half-maximum (FWHM) techniques. The accuracy and reproducibility of these techniques may be hindered in AS by the coexistence of diffuse interstitial fibrosis and the presence of relatively small, non-bright scars. The validation of these techniques against histology, which is the current gold standard for scar quantification in AS, is limited. Based on the best current evidence, the STRM method using a threshold of three standard deviations above the mean signal intensity of remote myocardium is recommended. The high reproducibility of the FWHM technique in non-AS cohorts has been shown and merits further evaluation within the context of AS. Future directions include the use of quantitative T1 mapping for the detection and quantification of scar, as well as the development of serum biomarkers that reflect the fibrotic status of the myocardium in AS. Full article

The evaluation and accurate diagnosis of the type and severity of aortic stenosis relies on the precision of medical imaging technology and clinical correlations and the expertise of medical professionals. The application of the clinical correlation to different aortic stenosis morphologies and severities is investigated. The manner in which numerical techniques can be used to simulate the blood flow through pathological aortic valves was analysed and compared to the ground-truth CFD model. Larger pressure gradients are estimated in all severities of rheumatic aortic valves compared to calcific aortic valves. The zero-dimensional morphology-insensitive model underpredicted the transvalvular pressure gradient with the greatest error. The 1D model underestimated the pressure gradient in rheumatic cases and overestimated the pressure gradient in calcific cases. The pressure gradients estimated by the clinical approach depends on the location of the flow vena contracta and is sensitive to the severity and type of valve lesion. Through the analysis of entropy generation within the flow domain, the dominant parameters and regions driving adverse pressure gradients were identified. It is concluded that sudden expansion is the dominant parameter leading to higher pressure gradients in rheumatic heart valves compared to calcific ones. Full article

Hypertensive crisis can present with cardiac troponin elevation and unobstructed coronary arteries. We used cardiac magnetic resonance (CMR) imaging to characterize the myocardial tissue in patients with hypertensive crisis, elevated cardiac troponin, and unobstructed coronary arteries. Patients with hypertensive crisis and elevated cardiac troponin with coronary artery stenosis <50% were enrolled. Patients with troponin-negative hypertensive crisis served as controls. All participants underwent CMR imaging at 1.5 Tesla. Imaging biomarkers and tissue characteristics were compared between the groups. There were 19 patients (63% male) with elevated troponin and 24 (33% male) troponin-negative controls. The troponin-positive group was older (57 ± 11 years vs. 47 ± 14 years, p = 0.015). The groups had similar T2-weighted signal intensity ratios and native T1 times. T2 relaxation times were longer in the troponin-positive group, and the difference remained significant after excluding infarct-pattern late gadolinium enhancement (LGE) from the analysis. Extracellular volume (ECV) was higher in the troponin-positive group (25 ± 4 ms vs. 22 ± 3 ms, p = 0.008) and correlated strongly with T2 relaxation time (r_s = 0.701, p = 0.022). Late gadolinium enhancement was 32% more prevalent in the troponin-positive group (82% vs. 50%, p = 0.050), with 29% having infarct-pattern LGE. T2 relaxation time was independently associated with troponin positivity (OR 2.1, p = 0.043), and both T2 relaxation time and ECV predicted troponin positivity (C-statistics: 0.71, p = 0.009; and 0.77, p = 0.006). Left ventricular end-diastolic and left atrial volumes were the strongest predictors of troponin positivity (C-statistics: 0.80, p = 0.001; and 0.82, p < 0.001). The increased T2 relaxation time and ECV and their significant correlation in the troponin-positive group suggest myocardial injury with oedema, while the non-ischaemic LGE could be due to myocardial fibrosis or acute necrosis. These CMR imaging biomarkers provide important clinical indices for risk stratification and prognostication in patients with hypertensive crisis. Full article

(1) Background: Altered cardiac morphology and function are associated with increased risks of adverse cardiac events in hypertension. Our study aimed to assess left ventricular (LV) morphology, geometry, and function using cardiovascular magnetic resonance (CMR) imaging in patients with hypertensive crisis. (2) Methods: Patients with hypertensive crisis underwent CMR imaging at 1.5 Tesla to assess cardiac volume, mass, function, and contrasted study. Left ventricular (LV) function and geometry were defined according to the guideline recommendations. Late gadolinium enhancement (LGE) was qualitatively assessed and classified into ischemic and nonischemic patterns. Predictors of LGE was determined using regression analysis. (3) Results: Eighty-two patients with hypertensive crisis (aged 48.5 ± 13.4 years, and 57% males) underwent CMR imaging. Of these patients, seventy-eight percent were hypertensive emergency and twenty-two percent were urgency. Diastolic blood pressure was higher under hypertensive emergency (p = 0.032). Seventy-nine percent (92% of emergency vs. 59% of urgency, respectively; p = 0.003) had left ventricular hypertrophy (LVH). The most prevalent LV geometry was concentric hypertrophy (52%). Asymmetric LVH occurred in 13 (22%) of the participants after excluding ischemic LGE. Impaired systolic function occurred in 46% of patients, and predominantly involved hypertensive emergency. Nonischemic LGE occurred in 75% of contrasted studies (67.2% in emergency versus 44.4% in urgency, respectively; p < 0.001). Creatinine and LV mass were independently associated with nonischemic LGE. (5) Conclusion: LVH, altered geometry, asymmetric LVH, impaired LV systolic function, and LGE are common under hypertensive crisis. LVH and LGE more commonly occurred under hypertensive emergency. Longitudinal studies are required to determine the prognostic implications of asymmetric LVH and LGE in hypertensive crisis. Full article

There is a growing interest in the role of biomarkers in differentiating hypertensive emergency from hypertensive urgency. This study aimed to determine the diagnostic utility of lactate dehydrogenase (LDH), high-sensitivity cardiac troponin T (hscTnT), and N-terminal prohormone of brain-type natriuretic peptide (NT-proBNP) for identifying hypertensive emergency. A diagnosis of hypertensive emergency was made based on a systolic blood pressure of ≥180 mmHg and/or a diastolic blood pressure of ≥110 mmHg with acute hypertension-mediated organ damage. The predictive value of LDH, hscTnT, NT-proBNP, and models of these biomarkers for hypertensive emergency was determined using the area under the receiver operator characteristic curve (AUC). There were 66 patients (66.7% male) with a hypertensive emergency and 16 (31.3% male) with hypertensive urgency. LDH, NT-proBNP, and hscTnT were significantly higher in hypertensive emergency. Serum LDH > 190 U/L and high creatinine were associated with hypertensive emergency. LDH had an AUC ranging from 0.87 to 0.92 for the spectrum of hypertensive emergencies, while hscTnT had an AUC of 0.82 to 0.92, except for neurological emergencies, in which the AUC was 0.72. NT-proBNP was only useful in predicting acute pulmonary edema (AUC of 0.89). A model incorporating LDH with hscTnT had an AUC of 0.92 to 0.97 for the spectrum of hypertensive emergencies. LDH in isolation or combined with hscTnT correctly identified hypertensive emergency in patients presenting with hypertensive crisis. The routine assessment of these biomarkers has the potential to facilitate the timely identification of hypertensive emergencies, especially in patients with subtle and subclinical target organ injury. Full article

Myocardial injury and myocardial infarction can complicate a hypertensive emergency, and both are associated with poor prognosis. However, little is known about the prevalence of myocardial injury and the different subtypes of myocardial infarction in patients with hypertensive emergencies. This systematic review aims to determine the prevalence of myocardial infarction and its subtypes, and the prevalence of myocardial injury in patients with hypertensive emergencies following the PRISMA guideline. A systematic search of PubMed, Web of Science, and EBSCOHost (MEDLINE) databases was carried out from inception to identify relevant articles. A total of 18 studies involving 7545 patients with a hypertensive emergency were included. Fifteen (83.3%) studies reported on the prevalence of myocardial infarction ranging from 3.6% to 59.6%, but only two studies specifically indicated the prevalence of ST-elevation and non-ST-elevation myocardial infarction. The prevalence of myocardial injury was obtained in three studies (16.7%) and ranged from 15% to 63%. Despite being common, very few studies reported myocardial injury and the subtypes of myocardial infarction among patients presenting with a hypertensive emergency, highlighting the need for more research in this area which will provide pertinent data to guide patient management and identify those at increased risk of major adverse cardiovascular events. Full article

Reliable quantification of pulmonary arterial pressure is essential in the diagnostic and prognostic assessment of a range of cardiovascular pathologies, including rheumatic heart disease, yet an accurate and routinely available method for its quantification remains elusive. This work proposes an approach to infer pulmonary arterial pressure based on scientific machine learning techniques and non-invasive, clinically available measurements. A 0D multicompartment model of the cardiovascular system was optimized using several optimization algorithms subject to forward-mode automatic differentiation. Measurement data were synthesized from known parameters to represent the healthy, mitral regurgitant, aortic stenosed, and combined valvular disease situations with and without pulmonary hypertension. Eleven model parameters were selected for optimization based on 95% explained variation in mean pulmonary arterial pressure. A hybrid Adam and limited-memory Broyden–Fletcher–Goldfarb–Shanno optimizer yielded the best results with input data including valvular flow rates, heart chamber volume changes, and systematic arterial pressure. Mean absolute percentage errors ranged from 1.8% to 3.78% over the simulated test cases. The model was able to capture pressure dynamics under hypertensive conditions with pulmonary arterial systole, diastole, and mean pressure average percentage errors of 1.12%, 2.49%, and 2.14%, respectively. The low errors highlight the potential of the proposed model to determine pulmonary pressure for diseased heart valves and pulmonary hypertensive conditions. Full article

While mortality in patients with hypertensive emergency has significantly improved over the past decades, the incidence and complications associated with acute hypertension-mediated organ damage have not followed a similar trend. Hypertensive emergency is characterized by an abrupt surge in blood pressure, mostly occurring in people with pre-existing hypertension to result in acute hypertension-mediated organ damage. Acute hypertension-mediated organ damage commonly affects the cardiovascular system, and present as acute heart failure, myocardial infarction, and less commonly, acute aortic syndrome. Elevated cardiac troponin with or without myocardial infarction is one of the major determinants of outcome in hypertensive emergency. Despite being an established entity distinct from myocardial infarction, myocardial injury has not been systematically studied in hypertensive emergency. The current guidelines on the evaluation and management of hypertensive emergencies limit the cardiac troponin assay to patients presenting with features of myocardial ischemia and acute coronary syndrome, resulting in underdiagnosis, especially of atypical myocardial infarction. In this narrative review, we aimed to give an overview of the epidemiology and pathophysiology of hypertensive emergencies, highlight challenges in the evaluation, classification, and treatment of hypertensive emergency, and propose an algorithm for the evaluation and classification of cardiac acute hypertension-mediated organ damage. Full article