BACKGROUND:Pericardial effusions are frequently caused by inflammatory diseases. In cases of serosal inflammation, which often present with concomitant systemic symptoms, cardiac tamponade can occur, requiring emergency drainage. Nevertheless, it is rare for the index presentation of a previously undiagnosed inflammatory disease to be with cardiac tamponade. CASE SUMMARY:We describe a case of a young woman who presented in the postpartum period with cardiac tamponade. Further investigations confirmed that the underlying diagnosis was systemic lupus erythematosus (SLE). DISCUSSION:SLE can be associated with pericardial effusion but rarely causes cardiac tamponade. Herein, we describe a case of an index presentation of SLE in the postpartum period with a large pericardial effusion and tamponade. Cardiac imaging showed myocardial edema, reflective of associated myocarditis. TAKE-HOME MESSAGES:SLE can present in the immediate postpartum period, and acute management of tamponade in this context includes drainage of the effusion and immunosuppressive therapy.

Abstract Aims Stress echocardiography is widely used to identify obstructive coronary artery disease (CAD). High accuracy is reported in expert hands but is dependent on operator training and image quality. The EVAREST study provides UK-wide data to evaluate real-world performance and accuracy of stress echocardiography. Methods and results Participants undergoing stress echocardiography for CAD were recruited from 31 hospitals. Participants were followed up through health records which underwent expert adjudication. Cardiac outcome was defined as anatomically or functionally significant stenosis on angiography, revascularization, medical management of ischaemia, acute coronary syndrome, or cardiac-related death within 6 months. A total of 5131 patients (55% male) participated with a median age of 65 years (interquartile range 57–74). 72.9% of studies used dobutamine and 68.5% were contrast studies. Inducible ischaemia was present in 19.3% of scans. Sensitivity and specificity for prediction of a cardiac outcome were 95.4% and 96.0%, respectively, with an accuracy of 95.9%. Sub-group analysis revealed high levels of predictive accuracy across a wide range of patient and protocol sub-groups, with the presence of a resting regional wall motion abnormalitiy significantly reducing the performance of both dobutamine (P < 0.01) and exercise (P < 0.05) stress echocardiography. Overall accuracy remained consistently high across all participating hospitals. Conclusion Stress echocardiography has high accuracy across UK-based hospitals and thus indicates stress echocardiography is being delivered effectively in real-world practice, reinforcing its role as a first-line investigation in the assessment of patients with stable chest pain.

Treatment of hypertension and its complications remains a major ongoing health care challenge. Around 25% of heart attacks in Europe are already attributed to hypertension and by 2025 up to 60% of the population will have hypertension. Physical inactivity has contributed to the rising prevalence of hypertension, but patients who exercise or engage in physical activity reduce their risk of stroke, myocardial infarction, and cardiovascular mortality. Hence, current international guidelines on cardiovascular disease prevention provide generic advice to increase aerobic activity, but physiological responses differ with blood pressure (BP) level, and greater reductions in BP across a population may be achievable with more personalized advice. We performed a systematic review of meta-analyses to determine whether there was sufficient evidence for a scientific Consensus Document reporting how exercise prescription could be personalized for BP control. The document discusses the findings of 34 meta-analyses on BP-lowering effects of aerobic endurance training, dynamic resistance training as well as isometric resistance training in patients with hypertension, high-normal, and individuals with normal BP. As a main finding, there was sufficient evidence from the meta-review, based on the estimated range of exercise-induced BP reduction, the number of randomized controlled trials, and the quality score, to propose that type of exercise can be prescribed according to initial BP level, although considerable research gaps remain. Therefore, this evidence-based Consensus Document proposes further work to encourage and develop more frequent use of personalized exercise prescription to optimize lifestyle interventions for the prevention and treatment of hypertension.

BACKGROUND Cardiogenic shock (CS) is a state of critical end-organ hypoperfusion due to a primary cardiac disorder. For people with refractory CS despite maximal vasopressors, inotropic support and intra-aortic balloon pump, mortality approaches 100%. Mechanical assist devices provide mechanical circulatory support (MCS) which has the ability to maintain vital organ perfusion, to unload the failing ventricle thus reduce intracardiac filling pressures which reduces pulmonary congestion, myocardial wall stress and myocardial oxygen consumption. This has been hypothesised to allow time for myocardial recovery (bridge to recovery) or allow time to come to a decision as to whether the person is a candidate for a longer-term ventricular assist device (VAD) either as a bridge to heart transplantation or as a destination therapy with a long-term VAD. OBJECTIVES To assess whether mechanical assist devices improve survival in people with acute cardiogenic shock. SEARCH METHODS We searched CENTRAL, MEDLINE (Ovid), Embase (Ovid) and Web of Science Core Collection in November 2019. In addition, we searched three trials registers in August 2019. We scanned reference lists and contacted experts in the field to obtain further information. There were no language restrictions. SELECTION CRITERIA Randomised controlled trials on people with acute CS comparing mechanical assist devices with best current intensive care management, including intra-aortic balloon pump and inotropic support. DATA COLLECTION AND ANALYSIS We performed data collection and analysis according to the published protocol. Primary outcomes were survival to discharge, 30 days, 1 year and secondary outcomes included, quality of life, major adverse cardiovascular events (30 days/end of follow-up), dialysis-dependent (30 days/end of follow-up), length of hospital stay and length of intensive care unit stay and major adverse events. We used the five GRADE considerations (study limitations, consistency of effect, imprecision, indirectness, and publication bias) to assess the quality of a body of evidence as it relates to the studies which contribute data to the meta-analyses for the prespecified outcomes Summary statistics for the primary endpoints were risk ratios (RR), hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs). MAIN RESULTS The search identified five studies from 4534 original citations reviewed. Two studies included acute CS of all causes randomised to treatment using TandemHeart percutaneous VAD and three studies included people with CS secondary to acute myocardial infarction who were randomised to Impella CP or best medical management. Meta-analysis was performed only to assess the 30-day survival as there were insufficient data to perform any further meta-analyses. The results from the five studies with 162 participants showed mechanical assist devices may have little or no effect on 30-day survival (RR of 1.01 95% CI 0.76 to 1.35) but the evidence is very uncertain. Complications such as sepsis, thromboembolic phenomena, bleeding and major adverse cardiovascular events were not infrequent in both the MAD and control group across the studies, but these could not be pooled due to inconsistencies in adverse event definitions and reporting. We identified four randomised control trials assessing mechanical assist devices in acute CS that are currently ongoing. AUTHORS' CONCLUSIONS There is no evidence from this review of a benefit from MCS in improving survival for people with acute CS. Further use of the technology, risk stratification and optimising the use protocols have been highlighted as potential reasons for lack of benefit and are being addressed in the current ongoing clinical trials.

Hypertensive pregnancy is associated with increased maternal cardiovascular risk in later life. A range of cardiovascular adaptations after pregnancy have been reported to partly explain this risk. We used multimodality imaging to identify whether, by midlife, any pregnancy-associated phenotypes were still identifiable and to what extent they could be explained by blood pressure. Participants were identified by review of hospital maternity records 5 to 10 years after pregnancy and invited to a single visit for detailed cardiovascular imaging phenotyping. One hundred seventy-three women (age, 42±5 years, 70 after normotensive and 103 after hypertensive pregnancy) underwent magnetic resonance imaging of the heart and aorta, echocardiography, and vascular assessment, including capillaroscopy. Women with a history of hypertensive pregnancy had a distinct cardiac geometry with higher left ventricular mass index (49.9±7.1 versus 46.0±6.5 g/m 2 ; P =0.001) and ejection fraction (65.6±5.4% versus 63.7±4.3%; P =0.03) but lower global longitudinal strain (−18.31±4.46% versus −19.94±3.59%; P =0.02). Left atrial volume index was also increased (40.4±9.2 versus 37.3±7.3 mL/m 2 ; P =0.03) and E:A reduced (1.34±0.35 versus 1.52±0.45; P =0.003). Aortic compliance (0.240±0.053 versus 0.258±0.063; P =0.046) and functional capillary density (105.4±23.0 versus 115.2±20.9 capillaries/mm 2 ; P =0.01) were reduced. Only differences in functional capillary density, left ventricular mass, and atrial volume indices remained after adjustment for blood pressure ( P <0.01, P =0.01, and P =0.04, respectively). Differences in cardiac structure and geometry, as well as microvascular rarefaction, are evident in midlife after a hypertensive pregnancy, independent of blood pressure. To what extent these phenotypic patterns contribute to cardiovascular disease progression or provide additional measures to improve risk stratification requires further study.

Abstract Background Stress echocardiography has become established as the most widely applied non-invasive imaging test for diagnosis of coronary artery disease within the UK. However, stress echocardiography has been substantially qualitative, rather than quantitative, based on visual wall motion assessment. For the first time, we have identified and validated quantitative descriptors of cardiac geometry and motion, extracted from ultrasound images acquired using contrast agents in an automated way. Purpose To establish whether these novel imaging features can be generated in an automated, quantifiable and reproducible way from images acquired with perfluoropropane contrast, as well as investigating how these extracted measures compare to those extracted from sulphur hexafluoride contrast and non-contrast studies. Methods 100 patients who received perfluoropropane contrast during their stress echocardiogram were recruited. Their stress echocardiography images were processed through a deep learning algorithm. Novel feature values were recorded and a subset of 10 studies were repeated. The automated measures of global longitudinal strain (GLS) and ejection fraction (EF) extracted from these images were compared to values previously extracted from sulphur hexafluoride contrast and non-contrast images using the same software. Results A full set of 31 novel imaging features were successfully extracted from 79 studies acquired using the perfluoropropane contrast agent with a dropout rate of 14% (n=92, 8 incomplete image sets). Repeated analysis in a subset of 10 perfluoropropane cases demonstrated excellent reproducibility of the extracted feature values (R2=1). Automated values of GLS and EF, at both rest (GLS = −16.4±4.8%, EF = 63±13%) and stress stages (GLS = −17.7±5.8%, EF = 68±11%), were extracted from 83 perfluoropropane studies, with a dropout rate of 16% (n=99, fewer incomplete sets as short axis view not required). The ranges of GLS and EF measures extracted from the perfluoropropane images were comparable to the other contrast studies (n=222) (Rest GLS = −16.8±5.8%, Rest EF = 63±10%; Stress GLS = −19.1±6.7%, Stress EF = 71±9%) and non-contrast studies (n=86) (Rest GLS = −15.7±5.3%, Rest EF = 57±10%; Stress GLS = −17.3±6.4%, Stress EF = 61±14%). Conclusions Novel features and clinically relevant measures were extracted from images acquired using perfluoropropane contrast for the first time in a fully automated and reproducible way using a deep learning algorithm. The analysis failure rate and generated measures are comparable to those extracted from images using other commonly used sulphur hexafluoride contrast agents and non-contrast stress echocardiography studies. These findings demonstrate that deep learning algorithms can be used for automated quantitative analysis of stress echocardiograms acquired using various contrast agents and in non-contrast studies to improve stress echocardiography practice. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Lantheus Medical Imaging, Inc.

Background Pregnancy complications such as preterm birth and fetal growth restriction are associated with altered prenatal and postnatal cardiac development. We studied whether there were changes related specifically to pregnancy hypertension. Methods and Results Left and right ventricular volumes, mass, and function were assessed at birth and 3 months of age by echocardiography in 134 term‐born infants. Fifty‐four had been born to mothers who had normotensive pregnancy and 80 had a diagnosis of preeclampsia or pregnancy‐induced hypertension. Differences between groups were interpreted, taking into account severity of pregnancy disorder, sex, body size, and blood pressure. Left and right ventricular mass indexed to body surface area (LVMI and RVMI) were similar in both groups at birth (LVMI 20.9±3.7 versus 20.6±4.0 g/m2, P=0.64, RVMI 17.5±3.7 versus 18.1±4.7 g/m2, P=0.57). However, right ventricular end diastolic volume index was significantly smaller in those born to hypertensive pregnancy (16.8±5.3 versus 12.7±4.7 mL/m2, P=0.001), persisting at 3 months of age (16.4±3.2 versus 14.4±4.8 mL/m2, P=0.04). By 3 months of age these infants also had significantly greater LVMI and RVMI (LVMI 24.9±4.6 versus 26.8±4.9 g/m2, P=0.04; RVMI 17.1±4.2 versus 21.1±3.9 g/m2, P<0.001). Differences in RVMI and right ventricular end diastolic volume index at 3 months, but not left ventricular measures, correlated with severity of the hypertensive disorder. No differences in systolic or diastolic function were evident. Conclusions Infants born at term to a hypertensive pregnancy have evidence of both prenatal and postnatal differences in cardiac development, with right ventricular changes proportional to the severity of the pregnancy disorder. Whether differences persist long term as well as their underlying cause and relationship to increased cardiovascular risk requires further study.

HomeJournal of the American Heart AssociationVol. 7, No. 10Do Young Women Need Treatment for Hypertension After Pregnancy Complications? Open AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citations ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toOpen AccessEditorialPDF/EPUBDo Young Women Need Treatment for Hypertension After Pregnancy Complications? Christina Y. L. Aye, DPhil, Einas Elmahi, MB, Henry Boardman, DPhil and Paul Leeson, PhD, FRCP Christina Y. L. AyeChristina Y. L. Aye Oxford Cardiovascular Clinical Research Facility, Department of Cardiovascular Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom Nuffield Department of Women's and Reproductive Health, John Radcliffe Hospital, University of Oxford, United Kingdom , Einas ElmahiEinas Elmahi Oxford Cardiovascular Clinical Research Facility, Department of Cardiovascular Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom , Henry BoardmanHenry Boardman Oxford Cardiovascular Clinical Research Facility, Department of Cardiovascular Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom and Paul LeesonPaul Leeson Oxford Cardiovascular Clinical Research Facility, Department of Cardiovascular Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom Originally published13 May 2018https://doi.org/10.1161/JAHA.118.009159Journal of the American Heart Association. 2018;7:e009159IntroductionPregnancy complications, such as hypertensive disorders of pregnancy, are well established as independent risk factors for cardiovascular diseases in later life in both the mother1, 2 and the offspring.3, 4 Studies of women from 1 to 40 years after childbirth consistently show increased rates of hypertension, ischemic heart disease, cerebrovascular disease, and cardiovascular mortality following a hypertensive pregnancy.1, 2 There is also evidence of a dose response according to the severity of hypertension during pregnancy. The risk of cardiac disease following gestational hypertension is associated with lower risk compared with early onset preeclampsia, particularly when complicated by preterm delivery.2In this issue of the Journal of the American Heart Association (JAHA), Egeland et al add a real‐world perspective of this risk by reporting findings on rate of medication use for hypertension over the 10 years after pregnancy. Importantly, these women were normotensive before pregnancy; therefore, the findings reflect new‐onset disease.5 The authors also consider other possible reasons for developing hypertension. They show that a pregnancy complication is the main explanation for medication use in more than a quarter of the young women being treated. These findings are based on a substantial Norwegian cohort of >60 000 women that was linked to the Norwegian Prescription Database. In agreement with previous studies, a hypertensive pregnancy in addition to a very preterm delivery, before 32 weeks of gestation, was associated with the highest hazard ratio for subsequent hypertension (age‐adjusted hazard ratio: 14.33; 95% confidence interval, 9.03–22.70) compared with pregnancies without hypertension.An explanation for the association between pregnancy complications, such as hypertensive disorders of pregnancy, and long‐term cardiovascular disease has been that they are expressions of the same disease process. This is supported by the fact that they share common risk factors such as high maternal age, diabetes mellitus (both prepregnancy and gestational), obesity, and renal disease.6, 7, 8, 9, 10, 11, 12 Mothers who develop complications may have an adverse underlying cardiovascular phenotype that could predate the affected pregnancy and that may deteriorate further during the acute systemic disturbance of the pregnancy complication.13 Defining this relationship is complex: Retrospective analysis is not without limitations, and adequately powered longitudinal studies from before conception to after childbirth are limited.14 Nevertheless, there appear to be links among prepregnancy blood pressure levels, hypertension during pregnancy, and later problems. A rare study of >3000 women found that ≈50% of differences in blood pressure several years after pregnancy were explained by blood pressure differences before pregnancy.15Simply attributing later cardiovascular risk to standard cardiovascular risk profiles in women who have pregnancy complications is, however, probably overly simplistic. These women appear to have distinct risk characteristics,16 including low age, autoimmune disease, nulliparity, or an increased interval between pregnancies (>10 years), that alter risk for pregnancy complications. In addition, multiple pregnancy, ethnicity (nonwhite), assisted conception, and change in paternity are relevant, suggesting that distinct genetic and immunological components may drive early risk. Egeland et al found a persistent excess risk of hypertension after adjusting for numerous prepregnancy and postpartum risk factors, and in analyses restricted to women with a healthy prepregnancy body mass index, hazard ratios observed were similar to those in the whole study population.5 An impact on fetal growth was also not required because small size for gestational age was, on its own, not a risk factor for hypertension. Consequently, pregnancy appears to be a "stress test" for a specific type of cardiovascular risk associated with earlier onset disease in seemingly healthy individuals at time of pregnancy.In summary, this study by Egeland et al provides further evidence that common pregnancy complications, such as a hypertensive pregnancy and preterm birth, identify women at higher risk of cardiovascular disease in later life. A major strength of the work is that it provides real‐world clinical relevance, reinforcing the message that hypertension risk after pregnancy is not benign but sufficient to warrant treatment within relatively short time periods. Furthermore, more than a quarter of the risk of needing medication is attributable to pregnancy complication alone rather than to any other identifiable risk factors. Pregnancy complications occur relatively early women's lives. Consequently, the presence of a pregnancy complication provides an opportunity to identify high‐risk women early and to offer primary prevention advice and intervention before end‐stage disease has become established.17 Studies aimed at understanding the mechanisms behind this increased risk may reveal novel targets that will have future benefit.DisclosuresNone.Footnotes*Correspondence to: Paul Leeson, PhD, FRCP, Oxford Cardiovascular Clinical Research Facility, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DU, United Kingdom. E‐mail: paul.[email protected]ox.ac.ukThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.References1 Bellamy L, Casas JP, Hingorani AD, Williams DJ. Pre‐eclampsia and risk of cardiovascular disease and cancer in later life: systematic review and meta‐analysis. BMJ. 2007; 335:974.CrossrefMedlineGoogle Scholar2 McDonald SD, Malinowski A, Zhou Q, Yusuf S, Devereaux PJ. Cardiovascular sequelae of preeclampsia/eclampsia: a systematic review and meta‐analyses. Am Heart J. 2008; 156:918–930.CrossrefMedlineGoogle Scholar3 Davis EF, Lewandowski AJ, Aye C, Williamson W, Boardman H, Huang RC, Mori TA, Newnham J, Beilin LJ, Leeson P. Clinical cardiovascular risk during young adulthood in offspring of hypertensive pregnancies: insights from a 20‐year prospective follow‐up birth cohort. BMJ Open. 2015; 5:e008136.CrossrefMedlineGoogle Scholar4 Davis EF, Lazdam M, Lewandowski AJ, Worton SA, Kelly B, Kenworthy Y, Adwani S, Wilkinson AR, McCormick K, Sargent I, Redman C, Leeson P. Cardiovascular risk factors in children and young adults born to preeclamptic pregnancies: a systematic review. Pediatrics. 2012; 129:e1552–e1561.CrossrefMedlineGoogle Scholar5 Egeland GM, Skurtveit S, Staff AC, Eide GE, Daltveit AK, Klungsøyr K, Trogstad L, Magnus PM, Brantsæter AL, Haugen M. Pregnancy‐related risk factors are associated with a significant burden of treated hypertension within 10 years of delivery: findings from a population‐based Norwegian cohort. J Am Heart Assoc. 2018; 7:e008318. DOI: 10.1161/JAHA.117.008318.LinkGoogle Scholar6 Toshimitsu M, Nagamatsu T, Nagasaka T, Iwasawa‐Kawai Y, Komatsu A, Yamashita T, Osuga Y, Fujii T. Increased risk of pregnancy‐induced hypertension and operative delivery after conception induced by in vitro fertilization/intracytoplasmic sperm injection in women aged 40 years and older. Fertil Steril. 2014; 102:1065–1070.e1061.CrossrefMedlineGoogle Scholar7 Ros HS, Cnattingius S, Lipworth L. Comparison of risk factors for preeclampsia and gestational hypertension in a population‐based cohort study. Am J Epidemiol. 1998; 147:1062–1070.CrossrefMedlineGoogle Scholar8 Duckitt K, Harrington D. Risk factors for pre‐eclampsia at antenatal booking: systematic review of controlled studies. BMJ. 2005; 330:565.CrossrefMedlineGoogle Scholar9 van Oostwaard MF, Langenveld J, Schuit E, Papatsonis DN, Brown MA, Byaruhanga RN, Bhattacharya S, Campbell DM, Chappell LC, Chiaffarino F, Crippa I, Facchinetti F, Ferrazzani S, Ferrazzi E, Figueiro‐Filho EA, Gaugler‐Senden IP, Haavaldsen C, Lykke JA, Mbah AK, Oliveira VM, Poston L, Redman CW, Salim R, Thilaganathan B, Vergani P, Zhang J, Steegers EA, Mol BW, Ganzevoort W. Recurrence of hypertensive disorders of pregnancy: an individual patient data metaanalysis. Am J Obstet Gynecol. 2015; 212:624.e621‐617.CrossrefMedlineGoogle Scholar10 Ursavas A, Karadag M, Nalci N, Ercan I, Gozu RO. Self‐reported snoring, maternal obesity and neck circumference as risk factors for pregnancy‐induced hypertension and preeclampsia. Respiration. 2008; 76:33–39.CrossrefMedlineGoogle Scholar11 Parazzini F, Bortolus R, Chatenoud L, Restelli S, Ricci E, Marozio L, Benedetto C. Risk factors for pregnancy‐induced hypertension in women at high risk for the condition. Italian Study of Aspirin in Pregnancy Group. Epidemiology. 1996; 7:306–308.CrossrefMedlineGoogle Scholar12 Li DK, Wi S. Changing paternity and the risk of preeclampsia/eclampsia in the subsequent pregnancy. Am J Epidemiol. 2000; 151:57–62.CrossrefMedlineGoogle Scholar13 Lazdam M, Davis EF, Lewandowski AJ, Worton SA, Kenworthy Y, Kelly B, Leeson P. Prevention of vascular dysfunction after preeclampsia: a potential long‐term outcome measure and an emerging goal for treatment. J Pregnancy. 2012; 2012:704146.CrossrefMedlineGoogle Scholar14 Harrison S, Petkovic G, Chevassut A, Brook L, Higgins N, Kenworthy Y, Selwood M, Snelgar T, Arnold L, Boardman H, Heneghan C, Leeson P, Redman C, Granne I. Oxfordshire women and their children's health (OxWATCH): protocol for a prospective cohort feasibility study. BMJ Open. 2015; 5:e009282.CrossrefMedlineGoogle Scholar15 Romundstad PR, Magnussen EB, Smith GD, Vatten LJ. Hypertension in pregnancy and later cardiovascular risk: common antecedents?Circulation. 2010; 122:579–584.LinkGoogle Scholar16 Lazdam M, de la Horra A, Diesch J, Kenworthy Y, Davis E, Lewandowski AJ, Szmigielski C, Shore A, Mackillop L, Kharbanda R, Alp N, Redman C, Kelly B, Leeson P. Unique blood pressure characteristics in mother and offspring after early onset preeclampsia. Hypertension. 2012; 60:1338–1345.LinkGoogle Scholar17 Rich‐Edwards JW, Fraser A, Lawlor DA, Catov JM. Pregnancy characteristics and women's future cardiovascular health: an underused opportunity to improve women's health?Epidemiol Rev. 2014; 36:57–70.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Lederer M, Wong A, Diego D, Nguyen D, Verma U and Chaturvedi S (2020) Tracking the Development of Cerebrovascular Risk Factors Following Pregnancy With Preeclampsia, Journal of Stroke and Cerebrovascular Diseases, 10.1016/j.jstrokecerebrovasdis.2020.104720, 29:6, (104720), Online publication date: 1-Jun-2020. May 15, 2018Vol 7, Issue 10Article InformationMetrics © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.https://doi.org/10.1161/JAHA.118.009159PMID: 29755037 Originally publishedMay 13, 2018 Keywordspreeclampsia/pregnancyEditorialspreventionPDF download SubjectsCardiovascular DiseasePregnancyPrimary PreventionWomen, Sex, and Gender

Commentary on: Gartlehner G, Patel SV, Feltner C, et al . Hormone Therapy for the Primary Prevention of Chronic Conditions in Postmenopausal Women: Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA 2017;318:2234–2249. There is a postmenopausal increase in the incidence of cognitive impairment, heart disease, osteoporosis, diabetes and some cancers. This has raised the question of whether hormone therapy can prevent chronic disease in asymptomatic postmenopausal women. Use of hormone therapy is associated with reduced cardiovascular and osteoporosis risk in observational studies.1 Subsequent large randomised controlled trials (RCT)2 3 cast doubt on these findings and raise concerns regarding an increased risk of harm in women randomised to receive hormone therapy. This systematic review and meta-analysis4 by the US Preventive Services Task Force (USPSTF) …

BACKGROUND Experimental and clinical studies show that prematurity leads to altered left ventricular (LV) structure and function with preserved resting LV ejection fraction (EF). Large-scale epidemiological data now links prematurity to increased early heart failure risk. OBJECTIVES The authors performed echocardiographic imaging at prescribed exercise intensities to determine whether preterm-born adults have impaired LV functional response to physical exercise. METHODS We recruited 101 normotensive young adults born preterm (n = 47; mean gestational age 32.8 +/- 3.2 weeks) and term (n = 54) for detailed cardiovascular phenotyping. Full clinical resting and exercise stress echocardiograms were performed, with apical 4-chamber views collected while exercising at 40%, 60%, and 80% of peak exercise capacity, determined by maximal cardiopulmonary exercise testing. RESULTS Preterm-born individuals had greater LV mass (p = 0.015) with lower peak systolic longitudinal strain (p = 0.038) and similar EF to term-born control subjects at rest (p = 0.62). However, by 60% exercise intensity, EF was 6.7% lower in preterm subjects (71.9 +/- 8.7% vs 78.6 +/- 5.4%; p = 0.004) and further declined to 7.3% below the term-born group at 80% exercise intensity (69.8 +/- 6.4% vs 77.1 +/- 6.3%; p = 0.004). Submaximal cardiac output reserve was 56% lower in preterm-born subjects versus term-born control subjects at 40% of peak exercise capacity (729 +/- 1,162 ml/min/m(2) vs. 1,669 +/- 937 ml/min/m(2); p = 0.021). LV length and resting peak systolic longitudinal strain predicted EF increase from rest to 60% exercise intensity in the preterm group (r = 0.68, p = 0.009 and r = 0.56, p = 0.031, respectively). CONCLUSIONS Preterm-born young adults had impaired LV response to physiological stress when subjected to physical exercise, which suggested a reduced myocardial functional reserve that might help explain their increased risk of early heart failure. (Young Adult Cardiovascular Health sTudy [YACHT]; NCT02103231) (c) 2018 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Background Heart rate variability (HRV) has emerged as a predictor of later cardiac risk. This study tested whether pregnancy complications that may have long-term offspring cardiac sequelae are associated with differences in HRV at birth, and whether these HRV differences identify abnormal cardiovascular development in the postnatal period. Methods Ninety-eight sleeping neonates had 5-min electrocardiogram recordings at birth. Standard time and frequency domain parameters were calculated and related to cardiovascular measures at birth and 3 months of age. Results Increasing prematurity, but not maternal hypertension or growth restriction, was associated with decreased HRV at birth, as demonstrated by a lower root mean square of the difference between adjacent NN intervals (rMSSD) and low (LF) and high-frequency power (HF), with decreasing gestational age ( p < 0.001, p = 0.009 and p = 0.007, respectively). We also demonstrated a relative imbalance between sympathetic and parasympathetic tone, compared to the term infants. However, differences in autonomic function did not predict cardiovascular measures at either time point. Conclusions Altered cardiac autonomic function at birth relates to prematurity rather than other pregnancy complications and does not predict cardiovascular developmental patterns during the first 3 months post birth. Long-term studies will be needed to understand the relevance to cardiovascular risk.

Importance:Risk of stroke and brain atrophy in later life relate to levels of cardiovascular risk in early adulthood. However, it is unknown whether cerebrovascular changes are present in young adults. Objective:To examine relationships between modifiable cardiovascular risk factors and cerebrovascular structure, function, and white matter integrity in young adults. Design, Setting, and Participants:A cross-sectional observational study of 125 young adults (aged 18-40 years) without clinical evidence of cerebrovascular disease. Data collection was completed between August 2014 and May 2016 at the University of Oxford, United Kingdom. Final data collection was completed on May 31, 2016. Exposures:The number of modifiable cardiovascular risk factors at recommended levels, based on the following criteria: body mass index (BMI) <25; highest tertile of cardiovascular fitness and/or physical activity; alcohol consumption <8 drinks/week; nonsmoker for >6 months; blood pressure on awake ambulatory monitoring <130/80 mm Hg; a nonhypertensive diastolic response to exercise (peak diastolic blood pressure <90 mm Hg); total cholesterol <200 mg/dL; and fasting glucose <100mg/dL. Each risk factor at the recommended level was assigned a value of 1, and participants were categorized from 0-8, according to the number of risk factors at recommended levels, with higher numbers indicating healthier risk categories. Main Outcomes and Measures:Cerebral vessel density, caliber and tortuosity, brain white matter hyperintensity lesion count. In a subgroup (n = 52), brain blood arrival time and cerebral blood flow assessed by brain magnetic resonance imaging (MRI). Results:A total of 125 participants, mean (SD) age 25 (5) years, 49% women, with a mean (SD) score of 6.0 (1.4) modifiable cardiovascular risk factors at recommended levels, completed the cardiovascular risk assessment and brain MRI protocol. Cardiovascular risk factors were correlated with cerebrovascular morphology and white matter hyperintensity count in multivariable models. For each additional modifiable risk factor categorized as healthy, vessel density was greater by 0.3 vessels/cm3 (95% CI, 0.1-0.5; P = .003), vessel caliber was greater by 8 μm (95% CI, 3-13; P = .01), and white matter hyperintensity lesions were fewer by 1.6 lesions (95% CI, -3.0 to -0.5; P = .006). Among the 52 participants with available data, cerebral blood flow varied with vessel density and was 2.5 mL/100 g/min higher for each healthier category of a modifiable risk factor (95% CI, 0.16-4.89; P = .03). Conclusions and Relevance:In this preliminary study involving young adults without clinical evidence of cerebrovascular disease, a greater number of modifiable cardiovascular risk factors at recommended levels was associated with higher cerebral vessel density and caliber, higher cerebral blood flow, and fewer white matter hyperintensities. Further research is needed to verify these findings and determine their clinical importance.

Objectives To study whether young adults with elevated blood pressure have an altered left ventricular stress response and whether this is determined by cardiac structure. Methods We recruited 148 young adults (mean age 27±5 years) with a range of blood pressures for cardiovascular phenotyping at rest with cardiac magnetic resonance. A subgroup (n=49) then underwent exercise stress echocardiography while exercising at 40%, 60%, and 80% of peak exercise capacity. Myocardial stress response was assessed from changes in ejection fraction and biochemistry (post-exercise copeptin release). Results were compared in participants with systolic or diastolic BP e 120/80 mm Hg (n=62, mean BP 129/77 mm Hg) vs. those with systolic and diastolic BP <120/80 mm Hg (n=84, mean BP 110/66 mm Hg). Results Resting left ventricular ejection fraction was similar between groups with higher or lower blood pressure. However, during physical exercise, despite similar achieved work load, higher blood pressure was associated with lower ejection fraction at 40% and 60% exercise load (73.9±3.25 vs. 80.0±4.54%, p<0.001 and 75.2±6.59 vs. 79.4±4.70%, p=0.026 respectively) as well as lower submaximal contractile reserve (10.4±5.92 vs. 19.0±6.90%, p<0.001 and 11.5±8.34 vs. 17.5±7.31%, p=0.029 at 40% and 60% respectively). Furthermore, increases in post-exercise plasma copeptin level were predicted by lower ejection fraction at 40% workload (beta=−0.329, p=0.045). Blood pressure was associated with variation in left ventricular mass index (55.6±10.0 vs. 52.0±9.6 g/m2, p=0.041 and 0.68±0.13 vs. 0.62±0.12 g/ml, p=0.007) and wall thickness (7.21±1.31 vs. 6.62±1.44 mm, p=0.015) but measures were within clinically normal ranges and did not predict variation in myocardial stress response. Conclusions x0013_Young adults with modest blood pressure elevation have a significantly lower systolic response to exercise. The association between this altered stress response and daily functional limitations in young adulthood, as well as cardiovascular disease progression and event risk, requires further study.

Pregnancy complications, such as hypertensive disorders or preterm delivery, identify families predisposed to cardiovascular problems at other times in life. Whether the pregnancy complication induces cardiac disease or whether the pregnancy stress unmasks an underlying predisposition remains unclear. However, improved survival following severe pregnancy complications for both the mother and, in particular, the offspring - who is often born preterm - has resulted in a growing cohort of individuals who carry this increased cardiovascular risk. Research to understand the underlying pathological mechanisms that link these conditions might ultimately lead to novel therapeutic or prevention strategies for both cardiovascular and pregnancy disease.