Search

Background: It is unclear how rising obesity among people with HIV (PWH) impacts their risk of type 2 diabetes mellitus (diabetes). We examined associations between HIV, prevalent diabetes and adiposity among South African PWH and their peers without HIV (PWOH)., Methods: HIV status was ascertained by antibody testing. Diabetes was defined as current use of oral hypoglycemics, insulin, and/or HbA1c ≥6.5%. Adiposity was measured by body mass index (BMI), waist circumference and waist-to-height ratio. Their associations were examined using sex-stratified multivariable fractional polynomial generalized linear models, reporting adjusted prevalence and prevalence ratios (adjPR)., Results: The mean age among 1,254 PWH and 4,381 PWOH was 41 years (95%CI 28, 56). The prevalence of diabetes among males was similar between PWH [11.3% (7.1, 15.5)] and PWOH [9.8% (8.5, 11.1); p=0.740]. By contrast, diabetes prevalence was higher among female PWOH [15.7% (14.4, 17.0)] than female PWH [10.5 (8.3, 12.8)%; adjPR: 0.67 (0.51, 0.82); p<0.001]. This difference was accentuated with obesity but reversed with leanness. At BMI ≥25 kg/m 2 , female PWH had lower diabetes prevalence [adjPR: 0.58 (0.41, 0.76); p<0.001] than female PHIV. In contrast, at BMI <18 kg/m 2 , female PWH had higher prevalence [adjPR: 1.72 (-1.53, 4.96); p=0.756] than female PWOH., Conclusion: We found sex-specific differences in the relationship between adiposity and diabetes prevalence by HIV serostatus in South Africa. Notably, females living with obesity and HIV had lower prevalence of diabetes than females living with obesity and without HIV, which may have particular implications for diabetes prevention programs in the region., Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2024.)

Background & Aims: Chronic liver disease (CLD) is associated with increased cardiovascular disease (CVD) risk. We investigated whether early signs of liver disease (measured by iron-corrected T1-mapping [cT1]) were associated with an increased risk of major CVD events., Methods: Liver disease activity (cT1) and fat (proton density fat fraction [PDFF]) were measured using LiverMultiScan® between January 2016 and February 2020 in the UK Biobank imaging sub-study. Using multivariable Cox regression, we explored associations between liver cT1 (MRI) and primary CVD (coronary artery disease, atrial fibrillation [AF], embolism/vascular events, heart failure [HF] and stroke), and CVD hospitalisation and all-cause mortality. Liver blood biomarkers, general metabolism biomarkers, and demographics were also included. Subgroup analysis was conducted in those without metabolic syndrome (defined as at least three of: a large waist, high triglycerides, low high-density lipoprotein cholesterol, increased systolic blood pressure, or elevated haemoglobin A1c)., Results: A total of 33,616 participants (mean age 65 years, mean BMI 26 kg/m 2 , mean haemoglobin A1c 35 mmol/mol) had complete MRI liver data with linked clinical outcomes (median time to major CVD event onset: 1.4 years [range: 0.002-5.1]; follow-up: 2.5 years [range: 1.1-5.2]). Liver disease activity (cT1), but not liver fat (PDFF), was associated with higher risk of any major CVD event (hazard ratio 1.14; 95% CI 1.03-1.26; p = 0.008), AF (1.30; 1.12-1.51; p <0.001); HF (1.30; 1.09-1.56; p= 0.004); CVD hospitalisation (1.27; 1.18-1.37; p <0.001) and all-cause mortality (1.19; 1.02-1.38; p = 0.026). FIB-4 index was associated with HF (1.06; 1.01-1.10; p = 0.007). Risk of CVD hospitalisation was independently associated with cT1 in individuals without metabolic syndrome (1.26; 1.13-1.4; p <0.001)., Conclusion: Liver disease activity, by cT1, was independently associated with a higher risk of incident CVD and all-cause mortality, independent of pre-existing metabolic syndrome, liver fibrosis or fat., Impact and Implications: Chronic liver disease (CLD) is associated with a twofold greater incidence of cardiovascular disease. Our work shows that early liver disease on iron-corrected T1 mapping was associated with a higher risk of major cardiovascular disease (14%), cardiovascular disease hospitalisation (27%) and all-cause mortality (19%). These findings highlight the prognostic relevance of a comprehensive evaluation of liver health in populations at risk of CVD and/or CLD, even in the absence of clinical manifestations or metabolic syndrome, when there is an opportunity to modify/address risk factors and prevent disease progression. As such, they are relevant to patients, carers, clinicians, and policymakers., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Little is known about the clinical characteristics, spectrum of causal genetic mutations and outcome of hypertrophic cardiomyopathy (HCM) in Africans. The objective of this study was to delineate the clinical and genetic features and outcome of HCM in African patients., Methods: Information on clinical presentation, electrocardiographic and echocardiographic findings, and outcome of cases with HCM was collected from the Cardiac Clinic at Groote Schuur Hospital over a mean duration of follow up of 9.1 ± 3.4 years. Genomic DNA was screened for mutations in 15 genes that cause HCM, i.e. cardiac myosin-binding protein C (MYBPC3), cardiac β-myosin heavy chain (MYH7), cardiac troponin T2 (TNNT2), cardiac troponin I (TNNI3), regulatory light chain of myosin (MYL2), essential light chain of myosin (MYL3), tropomyosin 1 (TPM1), phospholamban (PLN), α-actin (ACTC1), cysteine and glycine-rich protein 3 (CSRP3), AMP-activated protein kinase (PRKAG2), α-galactosidase (GLA), four-and-a-half LIM domains 1 (FHL1), lamin A/C (LMNA) and lysosome-associated membrane protein 2 (LAMP2). Survival and its predictors were analysed using the Kaplan-Meier and Cox proportional hazards regression methods, respectively., Results: Forty-three consecutive patients [mean age 38.5 ± 14.3 years; 25 (58.1%) male; and 13 (30.2%) black African] were prospectively enrolled in the study from January 1996 to December 2012. Clinical presentation was similar to that reported in other studies. The South African founder mutations that cause HCM were not found in the 42 probands. Ten of 35 index cases (28.6%) tested for mutations in 15 genes had disease-causing mutations in MYH7 (six cases or 60%) and MYBPC3 (four cases or 40%). No disease-causing mutation was found in the other 13 genes screened. The annual mortality rate was 2.9% per annum and overall survival was 74% at 10 years, which was similar to the general South African population. Cox's proportional hazards regression showed that survival was predicted by New York Heart Association (NYHA) functional class at last visit (p equals; 0.026), but not by the presence of a disease-causing mutation (p = 0.474)., Conclusions: Comprehensive genetic screening was associated with a 29% yield of causal genetic mutations in South African HCM cases, all in MYH7 and MBPC3 genes. A quarter of the patients had died after a decade of follow up, with NYHA functional class serving as a predictor of survival.

Pregnant women with known or suspected cardiovascular disease (CVD) often require cardiovascular imaging during pregnancy. The accepted maximum limit of ionising radiation exposure to the foetus during pregnancy is a cumulative dose of 5 rad. Concerns related to imaging modalities that involve ionising radiation include teratogenesis, mutagenesis and childhood malignancy. Importantly, no single imaging study approaches this cautionary dose of 5 rad (50 mSv or 50 mGy). Diagnostic imaging procedures that may be used in pregnancy include chest radiography, fluoroscopy, echocardiography, invasive angiography, cardiovascular computed tomography, computed tomographic pulmonary angiography, cardiovascular magnetic resonance (CMR) and nuclear techniques. Echocardiography and CMR appear to be completely safe in pregnancy and are not associated with any adverse foetal effects, provided there are no general contra-indications to MR imaging. Concerns related to safety of imaging tests must be balanced against the importance of accurate diagnosis and thorough assessment of the pathological condition. Decisions about imaging in pregnancy are premised on understanding the physiology of pregnancy, understanding basic concepts of ionising radiation, the clinical manifestations of existent CVD in pregnancy and features of new CVD. The cardiologist/physician must understand the indications for and limitations of, and the potential harmful effects of each test during pregnancy. Current evidence suggests that a single cardiovascular radiological study during pregnancy is safe and should be undertaken at all times when clinically justified. In this article, the different imaging modalities are reviewed in terms of how they work, how safe they are and what their clinical utility in pregnancy is. Furthermore, the safety of contrast agents in pregnancy is also reviewed.

Valvular heart disease poses a common yet difficult problem in everyday clinical practice. A thorough clinical evaluation with basic common investigations such as an electrocardiogram (ECG) and a chest radiograph (CXR) remains the cornerstone of diagnosis. Echocardiography and more invasive testing, if needed, are usually performed at specialist level to confirm the diagnosis, assess severity and assist in definitive decision-making.The causes and clinical, ECG and CXR features of the common valve lesions are described. Patients with symptomatic valve lesions should be referred for specialist assessment. In most cases, medical therapy serves as a bridge to definitive mechanical or surgical therapy.

Dyspnoea, also known as shortness of breath or breathlessness, is a subjective awareness of the sensation of uncomfortable breathing. It may be of physiological, pathological or social origin. The pathophysiology of dyspnoea is complex, and involves the activation of several pathways that lead to increased work of breathing, stimulation of the receptors of the upper or lower airway, lung parenchyma, or chest wall, and excessive stimulation of the respiratory centre by central and peripheral chemoreceptors. Activation of these pathways is relayed to the central nervous system via respiratory muscle and vagal afferents, which are consequently interpreted by the individual in the context of the affective state, attention, and prior experience, resulting in the awareness of breathing. The clinical evaluation and approach to the management of dyspnoea are directed by the clinical presentation and underlying cause. The causes of dyspnoea are manifold, and include a spectrum of disorders, from benign to serious and life-threatening entities. The pathophysiology, aetiology, clinical presentation and management of dyspnoea are reviewed.

Despite medical advances, heart failure (HF) remains a global health problem and sub-Saharan Africa (SSA) is no exception, with decompensated HF being the most common primary diagnosis for patients admitted to hospital with heart disease. In SSA the in-hospital mortality rate of decompensated HF is up to 8.3%. HF is a clinical syndrome that is caused by a diverse group of aetiologies, each requiring unique management strategies, highlighting the need for diagnostic certainty and a broad understanding of the complex pathophysiology of this condition. While there are a number of advanced medical, device and surgical interventions being tailored for HF internationally, the fundamental basic principles of HF management, such as patient education, effective management of congestion and initiation of disease-modifying medical therapies, remain a challenge on our continent. This review addresses both the epidemiology of HF in SSA and principles of management that focus specifically on symptom relief, prevention of hospitalisation and improving survival in this population.

Syncope, defined as a brief loss of consciousness due to an abrupt fall in cerebral perfusion, remains a frequent reason for medical presentation. The goals of the clinical assessment of a patient with syncope are twofold: (i) to identify the precise cause in order to implement a mechanism-specific and effective therapeutic strategy; and (ii) to quantify the risk to the patient, which depends on the underlying disease,rather than the mechanism of the syncope. Hence, a structured approach to the patient with syncope is required. History-taking remains the most important aspect of the clinical assessment. The classification of syncope is based on the underlying pathophysiological mechanism causing the event, and includes cardiac, orthostatic and reflex (neurally mediated) mechanisms. Reflex syncope can be categorised into vasovagal syncope (from emotional or orthostatic stress), situational syncope (due to specific situational stressors), carotid sinus syncope(from pressure on the carotid sinus, e.g. shaving or a tight collar), and atypical reflex syncope (episodes of syncope or reflex syncope that cannot be attributed to a specific trigger or syncope with an atypical presentation). Cardiovascular causes of syncope may be structural(mechanical) or electrical. Orthostatic hypotension is caused by an abnormal drop in systolic blood pressure upon standing, and is defined asa decrease of >20 mmHg in systolic blood pressure or a reflex tachycardia of >20 beats/minute within 3 minutes of standing. The main causes of orthostatic hypotension are autonomic nervous system failure and hypovolaemia. Patients with life-threatening causes of syncope should be managed urgently and appropriately. In patients with reflex or orthostatic syncope it is important to address any exacerbating medication and provide general measures to increase blood pressure, such as physical counter-pressure manoeuvres. Where heart disease is found to bet he cause of the syncope, a specialist opinion is warranted and where possible the problem should be corrected. It is important to remember that in any patient presenting with syncope the main objectives of management are to prolong survival, limit physical injuries and prevent recurrences. This can only be done if a patient is appropriately assessed at presentation, investigated as clinically indicated, and subsequently referred to a cardiologist for appropriate management.

Purpose: To investigate for the first time the feasibility of aortic four-dimensional (4D) flow at 7T, both contrast enhanced (CE) and non-CE. To quantify the signal-to-noise ratio (SNR) in aortic 4D flow as a function of field strength and CE with gadobenate dimeglumine (MultiHance)., Methods: Six healthy male volunteers were scanned at 1.5T, 3T, and 7T with both non-CE and CE acquisitions. Temporal SNR was calculated. Flip angle optimization for CE 4D flow was carried out using Bloch simulations that were validated against in vivo measurements., Results: The 7T provided 2.2 times the SNR of 3T while 3T provided 1.7 times the SNR of 1.5T in non-CE acquisitions in the descending aorta. The SNR gains achieved by CE were 1.8-fold at 1.5T, 1.7-fold at 3T, and 1.4-fold at 7T, respectively., Conclusion: The 7T provides a new tool to explore aortic 4D flow, yielding higher SNR that can be used to push the boundaries of acceleration and resolution. Field strength and contrast enhancement at all fields provide significant improvements in SNR., (© 2014 Wiley Periodicals, Inc.)

Background: Systemic sclerosis (SSc) is characterised by multi-organ tissue fibrosis including the myocardium. Diffuse myocardial fibrosis can be detected non-invasively by T1 and extracellular volume (ECV) quantification, while focal myocardial inflammation and fibrosis may be detected by T2-weighted and late gadolinium enhancement (LGE), respectively, using cardiovascular magnetic resonance (CMR). We hypothesised that multiparametric CMR can detect subclinical myocardial involvement in patients with SSc., Methods: 19 SSc patients (18 female, mean age 55 ± 10 years) and 20 controls (19 female, mean age 56 ± 8 years) without overt cardiovascular disease underwent CMR at 1.5T, including cine, tagging, T1-mapping, T2-weighted, LGE imaging and ECV quantification., Results: Focal fibrosis on LGE was found in 10 SSc patients (53%) but none of controls. SSc patients also had areas of myocardial oedema on T2-weighted imaging (median 13 vs. 0% in controls). SSc patients had significantly higher native myocardial T1 values (1007 ± 29 vs. 958 ± 20 ms, p < 0.001), larger areas of myocardial involvement by native T1 >990 ms (median 52 vs. 3% in controls) and expansion of ECV (35.4 ± 4.8 vs. 27.6 ± 2.5%, p < 0.001), likely representing a combination of low-grade inflammation and diffuse myocardial fibrosis. Regardless of any regional fibrosis, native T1 and ECV were significantly elevated in SSc and correlated with disease activity and severity. Although biventricular size and global function were preserved, there was impairment in the peak systolic circumferential strain (-16.8 ± 1.6 vs. -18.6 ± 1.0, p < 0.001) and peak diastolic strain rate (83 ± 26 vs. 114 ± 16 s-1, p < 0.001) in SSc, which inversely correlated with diffuse myocardial fibrosis indices., Conclusions: Cardiac involvement is common in SSc even in the absence of cardiac symptoms, and includes chronic myocardial inflammation as well as focal and diffuse myocardial fibrosis. Myocardial abnormalities detected on CMR were associated with impaired strain parameters, as well as disease activity and severity in SSc patients. CMR may be useful in future in the study of treatments aimed at preventing or reducing adverse myocardial processes in SSc.

Background: Cardiovascular magnetic resonance (CMR) is regarded as the gold standard for clinical assessment of the aorta, but normal dimensions are usually referenced to echocardiographic and computed tomography data and no large CMR normal reference range exists. As a result we aimed to 1) produce a normal CMR reference range of aortic diameters and 2) investigate the relationship between regional aortic size and body surface area (BSA) in a large group of healthy subjects with no vascular risk factors., Methods: 447 subjects (208 male, aged 19-70 years) without identifiable cardiac risk factors (BMI range 15.7-52.6 kg/m2) underwent CMR at 1.5 T to determine aortic diameter at three levels: the ascending aorta (Ao) and proximal descending aorta (PDA) at the level of the pulmonary artery, and the abdominal aorta (DDA), at a level 12 cm distal to the PDA. In addition, 201 of these subjects had aortic root imaging, allowing for measurements at the level of the aortic valve annulus (AV), aortic sinuses and sinotubular junction (STJ)., Results: Normal diameters (mean ±2 SD) were; AV annulus male(♂) 24.4 ± 5.4, female (♀) 21.0 ± 3.6 mm, aortic sinus♂ 32.4 ± 7.7, ♀27.6 ± 5.8 mm, ST-junction ♂25.0 ± 7.4, ♀21.8 ± 5.4 mm, Ao ♂26.7 ± 7.7, ♀25.5 ± 7.4 mm, PDA ♂20.6 ± 5.6, +18.9 ± 4.0 mm, DDA ♂17.6 ± 5.1, ♀16.4 ± 4.0 mm. Aortic root and thoracic aortic diameters increased at all levels measured with BSA. No gender difference was seen in the degree of dilatation with increasing BSA (p>0.5 for all analyses)., Conclusion: Across both genders, increasing body size is characterized by a modest degree of aortic dilatation, even in the absence of traditional cardiovascular risk factors.

Background: Quantitative T1-mapping is rapidly becoming a clinical tool in cardiovascular magnetic resonance (CMR) to objectively distinguish normal from diseased myocardium. The usefulness of any quantitative technique to identify disease lies in its ability to detect significant differences from an established range of normal values. We aimed to assess the variability of myocardial T1 relaxation times in the normal human population estimated with recently proposed Shortened Modified Look-Locker Inversion recovery (ShMOLLI) T1 mapping technique., Methods: A large cohort of healthy volunteers (n = 342, 50% females, age 11-69 years) from 3 clinical centres across two countries underwent CMR at 1.5T. Each examination provided a single average myocardial ShMOLLI T1 estimate using manually drawn myocardial contours on typically 3 short axis slices (average 3.4 ± 1.4), taking care not to include any blood pool in the myocardial contours. We established the normal reference range of myocardial and blood T1 values, and assessed the effect of potential confounding factors, including artefacts, partial volume, repeated measurements, age, gender, body size, hematocrit and heart rate., Results: Native myocardial ShMOLLI T1 was 962 ± 25 ms. We identify the partial volume as primary source of potential error in the analysis of respective T1 maps and use 1 pixel erosion to represent "midwall myocardial" T1, resulting in a 0.9% decrease to 953 ± 23 ms. Midwall myocardial ShMOLLI T1 was reproducible with an intra-individual, intra- and inter-scanner variability of ≤2%. The principle biological parameter influencing myocardial ShMOLLI T1 was the female gender, with female T1 longer by 24 ms up to the age of 45 years, after which there was no significant difference from males. After correction for age and gender dependencies, heart rate was the only other physiologic factor with a small effect on myocardial ShMOLLI T1 (6ms/10bpm). Left and right ventricular blood ShMOLLI T1 correlated strongly with each other and also with myocardial T1 with the slope of 0.1 that is justifiable by the resting partition of blood volume in myocardial tissue. Overall, the effect of all variables on myocardial ShMOLLI T1 was within 2% of relative changes from the average., Conclusion: Native T1-mapping using ShMOLLI generates reproducible and consistent results in normal individuals within 2% of relative changes from the average, well below the effects of most acute forms of myocardial disease. The main potential confounder is the partial volume effect arising from over-inclusion of neighbouring tissue at the manual stages of image analysis. In the study of cardiac conditions such as diffuse fibrosis or small focal changes, the use of "myocardial midwall" T1, age and gender matching, and compensation for heart rate differences may all help to improve the method sensitivity in detecting subtle changes. As the accuracy of current T1 measurement methods remains to be established, this study does not claim to report an accurate measure of T1, but that ShMOLLI is a stable and reproducible method for T1-mapping.

Introduction: Adenosine is the most widely used vasodilator stress agent for cardiovascular magnetic resonance (CMR) perfusion studies. With the standard dose of 140 mcg/kg/min some patients fail to demonstrate characteristic haemodynamic changes: a significant increase in heart rate (HR) and mild decrease in systolic blood pressure (SBP). Whether an increase in the rate of adenosine infusion would improve peripheral and, likely, coronary vasodilatation in those patients is unknown. The aim of the present study was to assess the tolerance and safety of a high-dose adenosine protocol in patients with inadequate haemodynamic response to the standard adenosine protocol when undergoing CMR perfusion imaging., Methods: 98 consecutive patients with known or suspected coronary artery disease (CAD) underwent CMR perfusion imaging at 1.5 Tesla. Subjects were screened for contraindications to adenosine, and an electrocardiogram was performed prior to the scan. All patients initially received the standard adenosine protocol (140 mcg/kg/min for at least 3 minutes). If the haemodynamic response was inadequate (HR increase < 10 bpm or SBP decrease < 10 mmHg) then the infusion rate was increased up to a maximum of 210 mcg/kg/min (maximal infusion duration 7 minutes)., Results: All patients successfully completed the CMR scan. Of a total of 98 patients, 18 (18%) did not demonstrate evidence of a significant increase in HR or decrease in SBP under the standard adenosine infusion rate. Following the increase in the rate of infusion, 16 out of those 18 patients showed an adequate haemodynamic response. One patient of the standard infusion group and two patients of the high-dose group developed transient advanced AV block. Significantly more patients complained of chest pain in the high-dose group (61% vs. 29%, p = 0.009). On multivariate analysis, age > 65 years and ejection fraction < 57% were the only independent predictors of blunted haemodynamic responsiveness to adenosine., Conclusions: A substantial number of patients do not show adequate peripheral haemodynamic response to standard-dose adenosine stress during perfusion CMR imaging. Age and reduced ejection fraction are predictors of inadequate response to standard dose adenosine. A high-dose adenosine protocol (up to 210 mcg/kg/min) is well tolerated and results in adequate haemodynamic response in nearly all patients.