Relationship of Subendocardial Perfusion to Myocardial Injury, Cardiac Structure, and Clinical Outcomes Among Patients With Hypertension.

BACKGROUND: Coronary microvascular dysfunction has been implicated in the development of hypertensive heart disease and heart failure, with subendocardial ischemia identified as a driver of sustained myocardial injury and fibrosis. We aimed to evaluate the relationships of subendocardial perfusion with cardiac injury, structure, and a composite of major adverse cardiovascular and cerebral events consisting of death, heart failure hospitalization, myocardial infarction, and stroke. METHODS: Layer-specific blood flow and myocardial flow reserve (MFR; stress/rest myocardial blood flow) were assessed by 13N-ammonia perfusion positron emission tomography in consecutive patients with hypertension without flow-limiting coronary artery disease (summed stress score <3) imaged at Brigham and Women's Hospital (Boston, MA) from 2015 to 2021. In this post hoc observational study, biomarkers, echocardiographic parameters, and longitudinal clinical outcomes were compared by tertiles of subendocardial MFR (MFRsubendo). RESULTS: Among 358 patients, the mean age was 70.6±12.0 years, and 53.4% were male. The median MFRsubendo was 2.57 (interquartile range, 2.08-3.10), and lower MFRsubendo was associated with older age, diabetes, lower renal function, greater coronary calcium burden, and higher systolic blood pressure (P<0.05 for all). In cross-sectional multivariable regression analyses, the lowest tertile of MFRsubendo was associated with myocardial injury and with greater left ventricular wall thickness and volumes compared with the highest tertile. Relative to the highest tertile, low MFRsubendo was independently associated with an increased rate of major adverse cardiovascular and cerebral events (adjusted hazard ratio, 2.99 [95% CI, 1.39-6.44]; P=0.005) and heart failure hospitalization (adjusted hazard ratio, 2.76 [95% CI, 1.04-7.32; P=0.042) over 1.1 (interquartile range, 0.6-2.8) years median follow-up. CONCLUSIONS: Among patients with hypertension without flow-limiting coronary artery disease, impaired MFRsubendo was associated with cardiovascular risk factors, elevated cardiac biomarkers, cardiac structure, and clinical events.

Hypertensive Heart Disease: Mechanisms, Diagnosis and Treatment.

Hypertensive heart disease (HHD) presents a substantial global health burden, spanning a spectrum from subtle cardiac functional alterations to overt heart failure. In this comprehensive review, we delved into the intricate pathophysiological mechanisms governing the onset and progression of HHD. We emphasized the significant role of neurohormonal activation, inflammation, and metabolic remodeling in HHD pathogenesis, offering insights into promising therapeutic avenues. Additionally, this review provided an overview of contemporary imaging diagnostic tools for precise HHD severity assessment. We discussed in detail the current potential treatments for HHD, including pharmacologic, lifestyle, and intervention devices. This review aimed to underscore the global importance of HHD and foster a deeper understanding of its pathophysiology, ultimately contributing to improved public health outcomes.

Deep Learning for Discrimination of Hypertrophic Cardiomyopathy and Hypertensive Heart Disease on MRI Native T1 Maps.

BACKGROUND: Native T1 and radiomics were used for hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD) differentiation previously. The current problem is that global native T1 remains modest discrimination performance and radiomics requires feature extraction beforehand. Deep learning (DL) is a promising technique in differential diagnosis. However, its feasibility for discriminating HCM and HHD has not been investigated. PURPOSE: To examine the feasibility of DL in differentiating HCM and HHD based on T1 images and compare its diagnostic performance with other methods. STUDY TYPE: Retrospective. POPULATION: 128 HCM patients (men, 75; age, 50 years ± 16) and 59 HHD patients (men, 40; age, 45 years ± 17). FIELD STRENGTH/SEQUENCE: 3.0T; Balanced steady-state free precession, phase-sensitive inversion recovery (PSIR) and multislice native T1 mapping. ASSESSMENT: Compare HCM and HHD patients baseline data. Myocardial T1 values were extracted from native T1 images. Radiomics was implemented through feature extraction and Extra Trees Classifier. The DL network is ResNet32. Different input including myocardial ring (DL-myo), myocardial ring bounding box (DL-box) and the surrounding tissue without myocardial ring (DL-nomyo) were tested. We evaluate diagnostic performance through AUC of ROC curve. STATISTICAL TESTS: Accuracy, sensitivity, specificity, ROC, and AUC were calculated. Independent t test, Mann-Whitney U-test and Chi-square test were adopted for HCM and HHD comparison. P < 0.05 was considered statistically significant. RESULTS: DL-myo, DL-box, and DL-nomyo models showed an AUC (95% confidential interval) of 0.830 (0.702-0.959), 0.766 (0.617-0.915), 0.795 (0.654-0.936) in the testing set. AUC of native T1 and radiomics were 0.545 (0.352-0.738) and 0.800 (0.655-0.944) in the testing set. DATA CONCLUSION: The DL method based on T1 mapping seems capable of discriminating HCM and HHD. Considering diagnostic performance, the DL network outperformed the native T1 method. Compared with radiomics, DL won an advantage for its high specificity and automated working mode. LEVEL OF EVIDENCE: 4 TECHNICAL EFFICACY STAGE: 2.

A study on the application of radiomics based on cardiac MR non-enhanced cine sequence in the early diagnosis of hypertensive heart disease.

BACKGROUND: The prevalence of hypertensive heart disease (HHD) is high and there is currently no easy way to detect early HHD. Explore the application of radiomics using cardiac magnetic resonance (CMR) non-enhanced cine sequences in diagnosing HHD and latent cardiac changes caused by hypertension. METHODS: 132 patients who underwent CMR scanning were divided into groups: HHD (42), hypertension with normal cardiac structure and function (HWN) group (46), and normal control (NOR) group (44). Myocardial regions of the end-diastolic (ED) and end-systolic (ES) phases of the CMR short-axis cine sequence images were segmented into regions of interest (ROI). Three feature subsets (ED, ES, and ED combined with ES) were established after radiomic least absolute shrinkage and selection operator feature selection. Nine radiomic models were built using random forest (RF), support vector machine (SVM), and naive Bayes. Model performance was analyzed using receiver operating characteristic curves, and metrics like accuracy, area under the curve (AUC), precision, recall, and specificity. RESULTS: The feature subsets included first-order, shape, and texture features. SVM of ED combined with ES achieved the highest accuracy (0.833), with a macro-average AUC of 0.941. AUCs for HHD, HWN, and NOR identification were 0.967, 0.876, and 0.963, respectively. Precisions were 0.972, 0.740, and 0.826; recalls were 0.833, 0.804, and 0.863, respectively; and specificities were 0.989, 0.863, and 0.909, respectively. CONCLUSIONS: Radiomics technology using CMR non-enhanced cine sequences can detect early cardiac changes due to hypertension. It holds promise for future use in screening for latent cardiac damage in early HHD.

Persistence of severe global inequalities in the burden of Hypertension Heart Disease from 1990 to 2019: findings from the global burden of disease study 2019.

AIMS: Assessing the global burden and health inequalities of Hypertension Heart Disease (HHD) during the period from 1990 to 2019. METHODS: Secondary analysis of the Global Burden of Disease (GBD) study in 2019, focusing on the burden of diseases, injuries, and risk factors worldwide. Disability-Adjusted Life Years (DALYs) data related to HHD are extracted from the 2019 GBD. Inequality Slope Index (SII) and Concentration Index are calculated to assess health inequalities across regions and countries. RESULTS: The total DALYs for HHD reached 21.51 million, demonstrating a substantial increase of 54.25% compared to the figures recorded in 1990, while the age-standardized DALY rates per 100,000 population for HHD in 2019 showed a notable decline to 268.19 (95% UI 204.57, 298.07), reflecting a significant decrease of 26.4% compared to the rates observed in 1990. The DALYs rate of hypertensive heart disease increases with age. Countries with moderate SDI accounted for 38.72% of the global burden of HHD in terms of DALYs. The highest age-standardized DALY rates (per 100,000) are predominantly concentrated in underdeveloped areas. In 1990 and 2019, the SII (per 100,000 population) for DALYs were - 121.6398 (95% CI -187.3729 to -55.90684) and - 1.592634 (95% CI -53.11027 to 49.925) respectively. The significant decline suggests a reduction in the inequality of age-standardized burden of HHD between high-income and low-income countries during this period. CONCLUSION: The unequal prevalence of HHD across different populations can hinder the achievement of the "health for all" objective. Persistent disparities in HHD have been observed globally over the past thirty years. It is crucial to prioritize efforts towards reducing avoidable health inequalities associated with hypertension-related heart disease, particularly in low-income and middle-income countries.

Obstructive Sleep Apnea and Hypertensive Heart Disease: From Pathophysiology to Therapeutics.

Obstructive sleep apnea (OSA) is characterized by recurrent episodes of complete or partial obstruction of the upper airway that lead to intermittent hypoxemia, negative intrathoracic pressure, hypercapnia, and sleep disturbances. While OSA is recognized as a significant risk factor for cardiovascular disease, it's relationship with hypertensive heart disease (HHD) remains underappreciated. HHD is a condition characterized by the pathological hypertrophy of the left ventricle, a consequence of elevated arterial hypertension. Interestingly, both OSA and HHD share similar underlying mechanisms including hypertension, left ventricular hypertrophy, myocardial fibrosis, oxidative stress, and inflammation, which ultimately contribute to the progression of HHD. This review aims to shed light on the potential role of OSA in HHD pathogenesis, summarizing current OSA treatment options. It is hoped that this review will encourage a renewed clinical focus on HHD and underscore the need for further OSA research, particularly in the context of screening and treating HHD patients.

An Integrated Algorithm for Differentiating Hypertrophic Cardiomyopathy From Hypertensive Heart Disease.

BACKGROUND: Differentiating hypertrophic cardiomyopathy (HCM) from hypertensive heart disease (HHD) is challenging. PURPOSE: To identify differences between HCM and HHD on a patient basis using MRI. STUDY TYPE: Retrospective. POPULATION: A total of 219 subjects, 148 in phase I (baseline data and algorithm development: 75 HCM, 33 HHD, and 40 controls) and 71 in phase II (algorithm validation: 56 HCM and 15 HHD). FIELD STRENGTH/SEQUENCE: Contrast-enhanced inversion-prepared gradient echo and cine-balanced steady-state free precession sequences at 3.0 T. ASSESSMENT: MRI parameters assessed included left ventricular (LV) ejection fraction (LVEF), LV end systolic and end diastolic volumes (LVESV and LVEDV), mean maximum LV wall thickness (MLVWT), LV global longitudinal and circumferential strain (GRS, GLS, and GCS), and native T1. Parameters, which were significantly different between HCM and HHD in univariable analysis, were entered into a principal component analysis (PCA). The selected components were then introduced into a multivariable regression analysis to model an integrated algorithm (IntA) for screening the two disorders. IntA performance was assessed for patients with and without LGE in phase I (development) and phase II (validation). STATISTICAL TESTS: Univariable regression, PCA, receiver operating curve (ROC) analysis. A P value <0.05 was considered statistically significant. RESULTS: Derived IntA formulation included LVEF, LVESV, LVEDV, MLVWT, and GCS. In LGE-positive subjects in phase l, the cutoff point of IntA ≥81 indicated HCM (83% sensitivity and 91% specificity), with the area under the ROC curve (AUC) of 0.900. In LGE-negative subjects, a higher possibility of HCM was indicated by a cutoff point of IntA ≥84 (100% sensitivity and 82% specificity), with an AUC of 0.947. Validation of IntA in phase II resulted in an AUC of 0.846 in LGE-negative subjects and 0.857 in LGE-positive subjects. DATA CONCLUSION: A per-patient-based IntA algorithm for differentiating HCM and HHD was generated from MRI data and incorporated FT, LGE and morphologic parameters. EVIDENCE LEVEL: 3. TECHNICAL EFFICACY: Stage 2.

Low coronary flow relative to myocardial mass predicts heart failure in symptomatic hypertensive patients with no obstructive coronary artery disease.

AIMS: The transition from hypertension to heart failure (HF) remains poorly understood. We hypothesized that insufficient perfusion to match global metabolic demand, reflected by a low ratio of myocardial blood flow to global myocardial mass, may be a HF risk marker. METHODS AND RESULTS: A retrospective cohort (n = 346) of patients with hypertension who underwent clinical positron emission tomography (PET) myocardial perfusion imaging for chest pain and/or dyspnoea at Brigham and Women's Hospital (Boston, MA, USA) were studied. Patients without obstructive coronary artery disease by history or PET perfusion (summed stress score <3), HF, cardiomyopathy, or ejection fraction (EF) <40% were followed for HF hospitalization (primary outcome), all-cause death, and their composite. Myocardial blood flow, left ventricular (LV) mass, volumes, and EF were obtained from PET, and a 'flow/mass ratio' was determined as hyperaemic myocardial blood flow over LV mass indexed to body surface area. A lower flow/mass ratio was independently associated with larger end-diastolic (ß = -0.44, P < 0.001) and end-systolic volume (ß = -0.48, P < 0.001) and lower EF (ß = 0.33, P < 0.001). A flow/mass ratio below the median was associated with an adjusted hazard ratio of 2.47 [95% confidence interval (CI) 1.24-4.93; P = 0.01] for HF hospitalization, 1.95 (95% CI 1.12-3.41; P = 0.02) for death, and 2.20 (95% CI 1.39-3.49; P < 0.001) for the composite. CONCLUSION: An integrated physiological measure of insufficient myocardial perfusion to match global metabolic demand identifies subclinical hypertensive heart disease and elevated risk of HF and death in symptomatic patients with hypertension but without flow-limiting coronary artery disease.

C-Reactive Protein Levels and Risk of Cardiovascular Diseases: A Two-Sample Bidirectional Mendelian Randomization Study.

Elevated C-reactive protein (CRP) levels are an indicator of inflammation, a major risk factor for cardiovascular disease (CVD). However, this potential association in observational studies remains inconclusive. We performed a two-sample bidirectional Mendelian randomization (MR) study using publicly available GWAS summary statistics to evaluate the relationship between CRP and CVD. Instrumental variables (IVs) were carefully selected, and multiple approaches were used to make robust conclusions. Horizontal pleiotropy and heterogeneity were evaluated using the MR-Egger intercept and Cochran's Q-test. The strength of the IVs was determined using F-statistics. The causal effect of CRP on the risk of hypertensive heart disease (HHD) was statistically significant, but we did not observe a significant causal relationship between CRP and the risk of myocardial infarction, coronary artery disease, heart failure, or atherosclerosis. Our primary analyses, after performing outlier correction using MR-PRESSO and the Multivariable MR method, revealed that IVs that increased CRP levels also increased the HHD risk. However, after excluding outlier IVs identified using PhenoScanner, the initial MR results were altered, but the sensitivity analyses remained congruent with the results from the primary analyses. We found no evidence of reverse causation between CVD and CRP. Our findings warrant updated MR studies to confirm the role of CRP as a clinical biomarker for HHD.

Coronary Microvascular Dysfunction and Hypertension: A Bond More Important than We Think.

Coronary microvascular dysfunction (CMD) is a clinical entity linked with various risk factors that significantly affect cardiac morbidity and mortality. Hypertension, one of the most important, causes both functional and structural alterations in the microvasculature, promoting the occurrence and progression of microvascular angina. Endothelial dysfunction and capillary rarefaction play the most significant role in the development of CMD among patients with hypertension. CMD is also related to several hypertension-induced morphological and functional changes in the myocardium in the subclinical and early clinical stages, including left ventricular hypertrophy, interstitial myocardial fibrosis, and diastolic dysfunction. This indicates the fact that CMD, especially if associated with hypertension, is a subclinical marker of end-organ damage and heart failure, particularly that with preserved ejection fraction. This is why it is important to search for microvascular angina in every patient with hypertension and chest pain not associated with obstructive coronary artery disease. Several highly sensitive and specific non-invasive and invasive diagnostic modalities have been developed to evaluate the presence and severity of CMD and also to investigate and guide the treatment of additional complications that can affect further prognosis. This comprehensive review provides insight into the main pathophysiological mechanisms of CMD in hypertensive patients, offering an integrated diagnostic approach as well as an overview of currently available therapeutical modalities.

Multimodal imaging shows fibrosis architecture and action potential dispersion are predictors of arrhythmic risk in spontaneous hypertensive rats.

Hypertensive heart disease (HHD) increases risk of ventricular tachycardia (VT) and ventricular fibrillation (VF). The roles of structural vs. electrophysiological remodelling and age vs. disease progression are not fully understood. This cross-sectional study of cardiac alterations through HHD investigates mechanistic contributions to VT/VF risk. Risk was electrically assessed in Langendorff-perfused, spontaneously hypertensive rat hearts at 6, 12 and 18 months, and paced optical membrane voltage maps were acquired from the left ventricular (LV) free wall epicardium. Distributions of LV patchy fibrosis and 3D cellular architecture in representative anterior LV mid-wall regions were quantified from macroscopic and microscopic fluorescence images of optically cleared tissue. Imaging showed increased fibrosis from 6 months, particularly in the inner LV free wall. Myocyte cross-section increased at 12 months, while inter-myocyte connections reduced markedly with fibrosis. Conduction velocity decreased from 12 months, especially transverse to the myofibre direction, with rate-dependent anisotropy at 12 and 18 months, but not earlier. Action potential duration (APD) increased when clustered by age, as did APD dispersion at 12 and 18 months. Among 10 structural, functional and age variables, the most reliably linked were VT/VF risk, general LV fibrosis, a measure quantifying patchy fibrosis, and non-age clustered APD dispersion. VT/VF risk related to a quantified measure of patchy fibrosis, but age did not factor strongly. The findings are consistent with the notion that VT/VF risk is associated with rate-dependent repolarization heterogeneity caused by structural remodelling and reduced lateral electrical coupling between LV myocytes, providing a substrate for heterogeneous intramural activation as HHD progresses. KEY POINTS: There is heightened arrhythmic risk with progression of hypertensive heart disease. Risk is related to increasing left ventricular fibrosis, but the nature of this relationship has not been quantified. This study is a novel systematic characterization of changes in active electrical properties and fibrotic remodelling during progression of hypertensive heart disease in a well-established animal disease model. Arrhythmic risk is predicted by several left ventricular measures, in particular fibrosis quantity and structure, and epicardial action potential duration dispersion. Age alone is not a good predictor of risk. An improved understanding of links between arrhythmic risk and fibrotic architectures in progressive hypertensive heart disease aids better interpretation of late gadolinium-enhanced cardiac magnetic resonance imaging and electrical mapping signals.

Hypertensive heart disease and myocardial fibrosis: How traditional Chinese medicine can help addressing unmet therapeutical needs.

Long-term elevated blood pressure will increase the cardiac load and lead to myocardial fibrosis (MF). A variety of pathological mechanisms and signal transduction pathways are involved in the process of hypertensive MF, which is of great significance for the occurrence and development of ventricular dilatation and heart failure. MF is the pathological basis of hypertensive heart disease (HHD), and blood pressure control is the key to delaying MF and reducing the occurrence of cardiovascular events. Although a large number of experimental results suggest that anti-MF drug therapy has made great progress, the conclusions of relevant clinical trials are still not optimistic, and it is urgent to find new effective anti-MF medicine. The clinical efficacy of traditional Chinese medicine (TCM) in the treatment of MF in HHD is obvious, and some achievements have been made in the mechanism research. Studies have confirmed that a variety of TCM compound prescription and natural compounds play different degrees of inhibitory effect on MF. In this study, we reviewed the pathogenesis of MF in HHD and the current drug treatment strategies, summarized the latest research progress of TCM in the treatment of MF in HHD, and demonstrated the mechanism of its cardiac protective effect. Finally, we pointed out the limitations of the current study and prospected the future research of TCM.

Newer Drugs to Reduce High Blood Pressure and Mitigate Hypertensive Target Organ Damage.

PURPOSE OF REVIEW: This review aims to investigate the blood pressure (BP)-lowering effects of emerging drugs developed to treat diabetic kidney disease and heart failure (HF). We summarize the potential pathophysiological mechanisms responsible for mitigating hypertensive target organ damage and evaluating the available clinical data on these newer drugs. RECENT FINDINGS: Nonsteroidal dihydropyridine-based mineralocorticoid receptor antagonists (MRAs), dual angiotensin II receptor-neprilysin inhibitors (valsartan with sacubitril), sodium-glucose cotransporter 2 inhibitors (SGLT2i), and soluble guanylate cyclase stimulators are new classes of chemical agents that have distinct mechanisms of action and have been shown to be effective for the treatment of cardiovascular (CV) disease (CVD), HF, and type 2 diabetes mellitus (T2D). These drugs can be used either alone or in combination with other antihypertensive and CV drugs. Among these, SGLT2i and valsartan with sacubitril offer new avenues to reduce CVD mortality. SGLT2i have a mild-to-moderate effect on BP lowering with a favorable effect on CV and renal hemodynamics and have been shown to produce a significant reduction in the incidence of major adverse CVD events (as monotherapy or add-on therapy) compared with controls (placebo or non-SGLT2i treatment). Most of the participants in these studies had hypertension (HTN) at baseline and were receiving antihypertensive therapy, including renin-angiotensin system blockers. The combination of valsartan with sacubitril also lowers BP in the short term and has demonstrated a striking reduction in CVD mortality and morbidity in HF patients with a reduced left ventricular ejection fraction. If widely adopted, these novel therapeutic agents hold significant promise for reducing the public health burden posed by HTN and CVD. Based on the results of several clinical trials and considering the high prevalence of HTN and T2D, these new classes of agents have emerged as powerful therapeutic tools in managing and lowering the BP of patients with diabetic kidney disease and HF.

Global, regional, and national burden of hypertensive heart disease during 1990-2019: an analysis of the global burden of disease study 2019.

BACKGROUND: Hypertensive heart disease (HHD) is a major public health issue worldwide. We analyzed the global, regional, and national burden of HHD between the years 1990 and 2019 in relation to age, gender, and socioeconomic factors. METHODS: The prevalence and death rates, the disability adjusted life-years (DALY), and the corresponding age-standardized rates of HHD were extracted from the Global Burden of Disease study 2019. The epidemiological trends were evaluated by calculating the estimated annual percentage changes (EAPC) of the above variates. RESULTS: A total of 19.60 million HHD cases were documented in 2019 compared to 7.82 million in 1990, corresponding to an EAPC of 0.17. Contrarily, the global age-standardized death rate (ASDR) and age-standardized DALYs decreased with respective EAPCs of - 0.74 and - 1.02. HHD mostly occurred in people aged over 65. The disease burden of HHD varied considerably between countries, and univariate linear regression indicated that many socioeconomic variables had significantly negative correlations with age-standardized DALY rate. CONCLUSION: HHD cases have increased over the last three decades; however the mortality rate has declined. Multi-faceted improvements in health, education and income could help to alleviate the disease burden of HHD, specially in some regions with lower socio-demographic index and higher ASDR.

Aortic stiffness and aortic-brachial stiffness mismatch as markers of renal dysfunction in hypertension.

PURPOSE: The dismal combination of hypertension and chronic kidney disease potentiates both cardiovascular disease and loss of renal function. Research points to the importance of arterial and left ventricular stiffening in this process but few studies have compared aspects of central and peripheral hemodynamics in relation to renal function in hypertension. MATERIALS AND METHODS: We investigated 107 hypertensive individuals with renal function ranging from normal to severe dysfunction with pulse wave analysis to obtain central blood pressures (BP), augmentation index, carotid-femoral and carotid-radial pulse wave velocity (cfPWV, crPWV), aortic-to-brachial stiffness mismatch (cfPWV/crPWV), endothelial function by forearm flow-mediated vasodilation and myocardial microvascular function by subendocardial viability ratio, and indices of left ventricular structure (left ventricular mass index and relative wall thickness, RWT) and diastolic function (left atrial volume index, E/A, and E/é). RESULTS: Mean age was 58 years, BP 149/87 mm Hg, 9% had cardiovascular disease, and 31% were on antihypertensive treatment. Mean estimated glomerular filtration rate (eGFR) was 74 (range 130-21) ml/min × 1.73 m2. Whereas cfPWV and cfPWV/crPWV were independently related to eGFR (r = -0.20, p = 0.002, r = -0.16, p = 0.01), central diastolic BP (r = 0.21, p = 0.04), RWT (r = -0.34, p = 0.001), E/é (r = -0.39, p < 0.001) and E/A (r = 0.27, p = 0.01) were related to eGFR in bivariate correlations, but these findings were not retained in multivariate analyses. Remaining markers of hypertensive heart disease and measures of microvascular function were not related to eGFR. CONCLUSION: Increased aortic stiffness and aortic-to-brachial stiffness mismatch are independently related to reduced eGFR in hypertensive patients, suggesting an important role for aortic stiffness in the evolution of hypertension-mediated renal dysfunction. Aortic stiffness and aortic-brachial stiffness mismatch may be useful early markers to find hypertensive patients at risk for decline in renal function.

Multi-parametric assessment of left ventricular hypertrophy using late gadolinium enhancement, T1 mapping and strain-encoded cardiovascular magnetic resonance.

AIM: To evaluate the ability of single heartbeat fast-strain encoded (SENC) cardiovascular magnetic resonance (CMR) derived myocardial strain to discriminate between different forms of left ventricular (LV) hypertrophy (LVH). METHODS: 314 patients (228 with hypertensive heart disease (HHD), 45 with hypertrophic cardiomyopathy (HCM), 41 with amyloidosis, 22 competitive athletes, and 33 healthy controls) were systematically analysed. LV ejection fraction (LVEF), LV mass index and interventricular septal (IVS) thickness, T1 mapping and atypical late gadolinium enhancement (LGE) were assessed. In addition, the percentage of LV myocardial segments with strain ≤ - 17% (%normal myocardium) was determined. RESULTS: Patients with amyloidosis and HCM exhibited the highest IVS thickness (17.4 ± 3.3 mm and 17.4 ± 6 mm, respectively, p < 0.05 vs. all other groups), whereas patients with amyloidosis showed the highest LV mass index (95.1 ± 20.1 g/m2, p < 0.05 vs all others) and lower LVEF compared to controls (50.5 ± 9.8% vs 59.2 ± 5.5%, p < 0.05). Analysing subjects with mild to moderate hypertrophy (IVS 11-15 mm), %normal myocardium exhibited excellent and high precision, respectively for the differentiation between athletes vs. HCM (sensitivity and specificity = 100%, Area under the curve; AUC%normalmyocardium = 1.0, 95%CI = 0.85-1.0) and athletes vs. HHD (sensitivity = 83%, specificity = 75%, AUC%normalmyocardium = 0.85, 95%CI = 0.78-0.90). Combining %normal myocardial strain with atypical LGE provided high accuracy also for the differentiation of HHD vs. HCM (sensitivity = 82%, specificity = 100%, AUCcombination = 0.92, 95%CI = 0.88-0.95) and HCM vs. amyloidosis (sensitivity = 83%, specificity = 100%, AUCcombination = 0.83, 95%CI = 0.60-0.96). CONCLUSION: Fast-SENC derived myocardial strain is a valuable tool for differentiating between athletes vs. HCM and athletes vs. HHD. Combining strain and LGE data is useful for differentiating between HHD vs. HCM and HCM vs. cardiac amyloidosis.

Spectrum of cardiovascular diseases at a referral tertiary care hospital in Somalia, Mogadishu: an echocardiographic study.

BACKGROUND: To investigate the frequencies and patterns of cardiovascular diseases (CVDs), including rheumatic and congenital heart diseases, among patients with abnormal hearts assessed by echocardiographic examination. METHODS: This retrospective, descriptive registry reviewed abnormal echocardiographic findings of 1140 patients aged 0-100 years who were admitted to the cardiology outpatient clinic at a tertiary training institution in Mogadishu. RESULTS: Hypertensive heart disease (HHD) (n:454, 39.8%), valvular heart disease (VHD) (n:395, 34.6%), and heart failure with reduced ejection fraction (HFrEF) (n:351, 30.8%) were the most frequent comorbidities. Congenital heart diseases (CHDs) were detected in 151 (13.2%) of the patients, with the most common ones including atrial septal defect (ASD) (n:37, 3.2%) and ventricular septal defect (VSD) (n:26, 2.3%). Rheumatic heart disease (RHD) was observed in 84 (7.4%) patients, among whom the most common age range was 16-30 years (40.5%), followed by 31-45 years (31%) and 0-15 years (15.5%). Mitral insufficiency (n:541, 47.5%) was detected as the most frequent VHD, followed by aortic insufficiency (n:437, 38.3%), and tricuspid insufficiency (n:264, 23.2%) and mitral valve stenosis (n:39, 3.4%) was the least common VHD. CONCLUSION: In the present study, we found that HHD was the most common comorbidity, followed by VHD, and HFrEF. Moreover, the most common VHD was mitral insufficiency and the most common CHD was ASD.

The role of overweight and obesity in adverse cardiovascular disease mortality trends: an analysis of multiple cause of death data from Australia and the USA.

BACKGROUND: In recent years, there have been adverse trends in premature cardiovascular disease (CVD) mortality rates (35-74 years) in the USA and Australia. Following long-term declines, rates in the USA are now increasing while falls in Australia have slowed rapidly. These two countries also have the highest adult obesity prevalence of high-income countries. This study investigates the role of overweight and obesity in their recent CVD mortality trends by using multiple cause of death (MCOD) data-direct individual-level evidence from death certificates-and linking the findings to cohort lifetime obesity prevalence. METHODS: We identified overweight- and obesity-related mortality as any CVD reported on the death certificate (CVD MCOD) with one or more of diabetes, chronic kidney disease, obesity, lipidemias or hypertensive heart disease (DKOLH-CVD), causes strongly associated with overweight and obesity. DKOLH-CVD comprises 50% of US and 40% of Australian CVD MCOD mortality. Trends in premature age-standardized death rates were compared between DKOLH-CVD and other CVD MCOD deaths (non-DKOLH-CVD). Deaths from 2000 to 2017 in the USA and 2006-2016 in Australia were analyzed. Trends in in age-specific DKOLH-CVD death rates were related to cohort relative lifetime obesity prevalence. RESULTS: Each country's DKOLH-CVD mortality rate rose by 3% per annum in the most recent year, but previous declines had reversed more rapidly in Australia. Non-DKOLH-CVD mortality in the USA increased in 2017 after declining strongly in the early 2000s, but in Australia it has continued declining in stark contrast to DKOLH-CVD. There were larger increases in DKOLH-CVD mortality rates at successively younger ages, strongly related with higher relative lifetime obesity prevalence in younger cohorts. CONCLUSIONS: The increase in DKOLH-CVD mortality in each country suggests that overweight and obesity has likely been a key driver of the recent slowdown or reversal of CVD mortality decline in both countries. The larger recent increases in DKOLH-CVD mortality and higher lifetime obesity prevalence in younger age groups are very concerning and are likely to adversely impact CVD mortality trends and hence life expectancy in future. MCOD data is a valuable but underutilized source of data to track important mortality trends.

A Contemporary Approach to Hypertensive Cardiomyopathy: Reversing Left Ventricular Hypertrophy.

PURPOSE OF REVIEW: To highlight pharmacological and non-pharmacological approaches to reversing hypertensive left ventricular hypertrophy (LVH). We identify high-risk phenotypes that may benefit from aggressive blood pressure (BP) management to prevent incident outcomes such as the development of atherosclerotic cardiovascular disease, stroke, and heart failure. RECENT FINDINGS: LVH is a modifiable risk factor. Intensive BP lowering (systolic BP < 120 mmHg) induces greater regression of electrocardiographic LVH than standard BP targets. The optimal agents for inducing LVH regression include renin-angiotensinogen-aldosterone system inhibitors and calcium channel blockers, although recent meta-analyses have demonstrated superior efficacy of non-hydrochlorothiazide diuretics. Novel agents (such as sacubitril/valsartan) and non-pharmacological approaches (like bariatric surgery) hold promise but longitudinal studies assessing their impact on clinical outcomes are needed. LVH regression is achievable with appropriate therapy with first-line antihypertensive agents. Additional studies are warranted to assess if intensive BP lowering in high-risk groups (such as blacks, women, and malignant LVH) improves outcomes.

Autoantibody profiling on a plasmonic nano-gold chip for the early detection of hypertensive heart disease.

The role of autoimmunity in cardiovascular (CV) diseases has been increasingly recognized. Autoimmunity is most commonly examined by the levels of circulating autoantibodies in clinical practices. Measurement of autoantibodies remains, however, challenging because of the deficiency of reproducible, sensitive, and standardized assays. The lack of multiplexed assays also limits the potential to identify a CV-specific autoantibody profile. To overcome these challenges, we developed a nanotechnology-based plasmonic gold chip for autoantibody profiling. This approach allowed simultaneous detection of 10 CV autoantibodies targeting the structural myocardial proteins, the neurohormonal regulatory proteins, the vascular proteins, and the proteins associated with apoptosis and coagulation. Autoantibodies were measured in four groups of participants across the continuum of hypertensive heart diseases. We observed higher levels of all 10 CV autoantibodies in hypertensive subjects (n = 77) compared with healthy participants (n = 30), and the autoantibodies investigated were related to each other, forming a highly linked network. In addition, we established that autoantibodies to troponin I, annexin-A5, and beta 1-adrenegic receptor best discriminated hypertensive subjects with adverse left ventricular (LV) remodeling or dysfunction (n = 49) from hypertensive subjects with normal LV structure and function (n = 28). By further linking these three significant CV autoantibodies to the innate and growth factors, we revealed a positive but weak association between autoantibodies to troponin I and proinflammatory cytokine IL-18. Overall, we demonstrated that this platform can be used to evaluate autoantibody profiles in hypertensive subjects at risk for heart failure.