These risks should be discussed, not only with the patient before she embarks on any assisted reproduction programme but also with the cardiology team looking after the patient so as to best manage the risks. Risks to the foetus that need to be discussed are the effects of drugs that may need to be continued and the possibility of miscarriage, prematurity, intra-uterine growth restriction and low birth weight and its implications. Detailed pre-conception counselling is especially important in the case of anticoagulation this aspect will be discussed in more detail further in the text.
It is also important to consider the likelihood of recurrence of the disease in the case of inherited cardiac conditions and congenital heart disease. In autosomal dominant conditions, such as Marfan syndrome, many patients are aware of the inheritance risk as family members are commonly affected. However, many patients are unaware of the inheritance risk of congenital heart disease and often assume it to be higher than it is.
The most heritable lesions are left-sided obstructive conditions, such as bicuspid aortic valve disease and coarctation, and the least heritable are the transposition complexes [ 21 — 26 ]. There is some evidence that pre-conception multivitamins and folic acid supplementation reduces the risk of heritable congenital heart disease in the foetus [ 23 , 24 ]. Factors that increase the risk of maternal cardiac events include left heart obstructive lesions aortic or mitral stenosis , cardiac symptoms, cyanosis, systemic ventricular impairment and previous cardiac events.
Atrioventricular valve regurgitation mitral or tricuspid also confers an increased risk. However, the most high-risk situation is the presence of a mechanical valve and the associated risk of full anticoagulation. Modified World Health Organisation system for risk assessment of cardiac conditions in pregnancy. After the key phase of pre-assessment, and care focusses on the assessment during pregnancy and the management of specific conditions.
Cardiac assessment of the pregnant patient can be difficult as common symptoms of pregnancy, such as breathlessness and fatigue, can mimic cardiac symptoms. Also, clinical signs, such as mild dependent oedema, a minimally raised jugular venous pressure, collapsing pulses and an ejection systolic murmur, are common in pregnancy and can result in difficult assessments [ 28 ].
Subtle changes in the ECG are common in later pregnancy and include left axis deviation, inverted T waves and inferior Q waves due to diaphragmatic elevation [ 30 ]. Chest radiography is a safe investigation modality in pregnancy and should be performed readily as required [ 31 ]. After the ECG, the most common investigation that most cardiologists will utilise is the echocardiogram, which is based on ultrasound and therefore safe throughout the pregnancy.
As would be predicted from the changes in maternal physiology, there is an observable increase in left ventricular diameter measurements on echocardiography, such as the left ventricular end diastolic and systolic dimensions [ 32 ]. Assessment of ventricular function is made utilising identical techniques to those used in the non-pregnant women, with ejection fraction, tissue Doppler and m-mode measurements all useful in serial monitoring.
There have been some inconsistencies in the reporting of alterations in measurements during the pregnancy period, with some studies reporting no change and others reporting a small drop late in pregnancy [ 32 , 33 ]. When assessing left ventricular function there does seem to be agreement across several studies that later in pregnancy the left ventricle becomes more globular in shape, accompanied by a drop in left ventricular longitudinal function and strain [ 32 , 34 , 35 ]; this would be in keeping with the late rise in afterload caused by the slight increase in SVR [ 34 ].
In the assessment of valvular lesions using echocardiography, pregnancy-related changes can often affect the severity of a valve lesion or the measurement made by echocardiography. In the context of stenotic valvular lesions, the extra volume load and heart rate increase seen in pregnancy can lead to an increase in the gradient measured across a valve without any observable change in the valve area measured by, for example, the continuity equation [ 36 ]. When measuring valve regurgitation, it is important to note that the extra volume load in pregnancy leads to an increase in observable tricuspid regurgitation without necessarily any change in the valve function; in contrast, mitral regurgitation, despite the extra volume load, often appears less during pregnancy due to the drop in SVR [ 37 ].
It is important for cardiologists to undertake serial scans and look at trends in valve pathology, and these changes need to be accompanied by clinical assessment. Cross-sectional imaging can be extremely valuable in diagnosis and surveillance during pregnancy. Cardiac magnetic resonance imaging is safe after the first trimester although gadolinium injection is not used due to a lack of data on its safety [ 38 ]. Computed tomography involves ionising radiation but may be required in spite of this drawback in life-threatening scenarios, such as a concern about aortic dissection or pulmonary embolus.
Cardiac catheterisation should be avoided in pregnancy but if required for example in emergency pacing the radiation dose should be minimised as much as possible and lead shielding used across the abdomen to reduce foetal exposure [ 39 ]. Specific guidance on some of the more commonly encountered conditions and important high-risk conditions are discussed in this section. The normal physiological changes of pregnancy of increased heart rate, cardiac output and circulating volume are particularly problematic for women with impaired systemic ventricular function.
Some women who are not diagnosed prior to pregnancy may be erroneously diagnosed with asthma or respiratory tract infections before the diagnosis of cardiomyopathy is made. Ventricular dysfunction due to ischaemic heart disease is very uncommon; most women have familial or idiopathic dilated cardiomyopathy. Some may have had previous chemotherapy or previous peripartum cardiomyopathy. Diagnosis is made clinically and most commonly in conjunction with echocardiography, with dysfunction often seen as a worsening on serial echocardiography.
Heart failure symptoms in pregnancy should be managed with rest and, as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are contraindicated, a combination of hydralazine and nitrate can be used to reduce cardiac afterload. Some women may need diuretics, although due to the pregnancy-related increase in glomerular filtration rate, fewer diuretics than normal may be needed. Beta-blockers can also be a useful adjunct therapy, and cardo-selective beta-blockers, such as bisoprolol and metoprolol, are more preferred.
Regular foetal growth scans are needed. Careful assessment of the likelihood of the pregnancy reaching viability needs to be assessed, and occasionally the decision may be made that continuing the pregnancy represents too high a risk to the mother, with advice that the pregnancy be terminated on medical grounds. Women may require in-patient treatment and rest, and early delivery may be needed. Prognosis in pregnancy for ventricular dysfunction as illustrated earlier based on data in the WHO scoring system and others is dependent on the level of ventricular dysfunction and symptom severity [ 27 , 42 ].
The aetiology is unknown, and there is a wide geographical variation in frequency, with countries such as Haiti having a particularly high prevalence. Recent experimental work suggests a potential pathogenic role for prolactin [ 44 ] and an overlap with hypertensive disorders and pre-eclampsia [ 45 ]. Treatment should be as for other types of heart failure. Bromocriptine, a prolactin-blocking drug, has been used on a case-by-case basis [ 46 ] and in a small trial [ 47 ], with some positive results and is currently undergoing testing in a larger randomised control trial.
The drug has the disadvantage of precluding breast-feeding [ 47 ], and there maybe some evidence that breast-feeding improves recovery in PPCM [ 48 ]. Prompt echocardiography is essential for early diagnosis, and a low index of suspicion for the condition is needed.
Response to treatment varies widely, with some women recovering fully and some requiring heart transplantation or even dying. Left ventricular recovery and survival differs between ethnic groups, with African—American women doing worse than Caucasians despite comparable treatment [ 51 ]. To date there are insufficient data available worldwide on the incidence of other obstructive lesions, such subvalvular or supravalvular lesions or hypertrophic cardiomyopathy with an obstructive gradient. Due to the extra volume load and inability to increase cardiac output across a fixed obstruction associated with both aortic and mitral stenosis, these conditions are significantly problematic during pregnancy and carry a high risk of morbidity and mortality [ 53 , 54 ].
Symptoms and signs often include increasing breathlessness, fatigue and oedema, and diagnosis if unknown prior to conception is usually confirmed with echocardiography. For mitral stenosis, the mainstay of treatment is rest, beta-blockade and diuretics for heart failure symptoms. Percutaneous balloon valvuloplasty has been widely used in rheumatic mitral stenosis and should be performed readily if the woman develops symptoms or foetal growth is compromised [ 55 ]. Aortic stenosis is better tolerated but often more problematic as the options for treatment are limited.
It is often due to bicuspid valve disease, and the results from balloon valvuloplasty are not so predictable or successful. Diuresis is not helpful, nor is beta-blockade. In both conditions, there is an increased risk of prematurity and intra-uterine growth restriction [ 56 ]. In moderate mitral stenosis and severe aortic stenosis, decisions around delivery often need to be made on a week by week basis as pregnancy progresses.
Many women experience palpitations during pregnancy that are not of clinical concern, but a small number of women with pre-existing or new diagnosed rhythm disorders may need treatment during pregnancy. Initial management should be as for any other patient with rhythm disorder: Safe therapies for tachyarrhythmias during pregnancy include adenosine, digoxin, flecainide and verapamil. Beta-blockers can cause intra-uterine growth restriction, but they are an effective therapy against most tachyarrhythmias in pregnancy.
In the context of clinical compromise and haemodynamic instability, electrical cardioversion should be used as normal, and no detrimental effects have been reported on the foetus due to electrical cardioversion, although foetal assessment afterwards is recommended [ 58 ].
Atrial fibrillation should be managed as in the non-pregnant patient, with attention paid to the need, or not, for anti-coagulation prior to or following a cardioversion. Catheter ablation is reserved for drug-resistant arrhythmias leading to haemodynamic compromise or refractory symptoms and if needed can be performed without fluroscopy [ 59 ]. VAs in women with heart disease occur most commonly late in pregnancy, usually in the third trimester with symptoms of heart failure [ 60 ].
Management, as stated earlier, should be as for the non-pregnant woman, with medications amiodarone avoided and defibrillator [implanted cardioverter defibrillator ICD ] therapy as needed or emergency cardioversion. Pregnancy itself does not seem to lead to an excess of ICD therapies [ 61 ]. Congenital long QT syndromes are associated with a risk of syncope and ventricular arrhythmias and a small risk of sudden death. It is safe to go through pregnancy with an ICD and important not to switch the device off during delivery.
If Caesarean section is required unipolar diathermy should be avoided. Bradyarrhythmias are much less common in pregnancy, and permanent pacing is rarely required [ 63 ]; however, if required, radiation exposure should be minimised. Some units have suggested isoproterenol can be used safely if needed in an emergency situation [ 64 ]. However, atherosclerotic coronary artery disease, which is the major burden of acquired cardiovascular disease worldwide, is becoming an increasing problem in pregnancy as women with traditional cardiovascular risk factors are becoming pregnant at an older age [ 66 ].
Pregnant women presenting with chest pain should be assessed in the usual way with an ECG and appropriate biomarkers, such as troponin. Traditional risk factors do determine the risk in the pregnant woman in the same way as in the normal population, and these should be used in the risk assessment. Treatment of an acute myocardial infarction should proceed as normal, with emergency angioplasty used per guidelines with bare metal stents as these have the widest historical evidence base in the pregnant woman [ 2 ].
Thrombolysis should not be performed as coronary artery dissection is so often the cause. Clopidogrel as a dual anti-platelet may be added to the therapeutic regimen for use in as short a course as possible following stenting; there is currently no evidence available for prasugrel or ticagrelor.
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If clopidogrel is prescribed, then the administration of an epidural is not safe. Although the above caveats need to be borne in mind, the most important part of management is to treat the mother in the most effective way possible to save her life. In developed countries, most women seen in cardiac—obstetric clinics have congenital heart disease [ 67 ].
Due to advances in cardiac surgery and paediatric intensive care almost all children born with congenital heart disease now survive to adulthood, with increasingly complex conditions. Many of these children want themselves to have children. Given the wide spectrum of lesions and repairs, women with congenital heart disease should be managed jointly between obstetricians and specialist cardiologists.
This spectrum of disorders in pregnancy is reviewed in detail elsewhere [ 68 ]. Aortopathies, such as Marfan syndrome, present a significant risk in pregnancy, with increased blood volume and vascular histological changes leading to increased risks of dissection.
Dissection most commonly occurs in the third trimester and in the post-partum period, and those patients with dilated aortas and a family history of dissection are at greatest risk. Type B dissection is unpredictable. Frequent surveillance by ECG during pregnancy is important, and the dissection risk can be reduced by beta-blockade [ 69 ]. Delivery should be highly medicalised with a combined spinal—epidural and passive second stage.
Very high-risk cases may need Caesarean section in cardiac theatres. Women should remain in hospital for 1 week after delivery. Women with dilated aortas in the context of a bicuspid aortic valve are at much less risk of dissection [ 70 ], although regular surveillance by ECG during pregnancy is still important, and beta-blockade and a medicalised delivery may be recommended if the aorta is particularly dilated. The mechanisms linking obesity to cardiac structural and functional abnormalities are not well understood. A complex interplay exists between body weight and haemodynamic, neurohormonal, and metabolic factors as well as inflammation and oxidative stress.
The association between body weight and heart failure was strongest in patients with conditions well known to be associated with heart failure CHD, diabetes, or hypertension and weakest, but still highly significant, in patients with valvular disease. There was also a strong association for heart failure attributed to cardiomyopathy, although this is a highly heterogeneous condition. With respect to limitations to our findings, diagnoses of heart failure, and other conditions were collected for administrative reasons, cases were not formally validated, and there was no data on cardiac function or other clinical characteristics.
Nonetheless, a hospital diagnosis of heart failure in Sweden has been shown to have high validity, particularly as a main diagnosis, 25 and so have other major cardiovascular diagnoses. In a recent unpublished validation study that we performed on hospital records with a discharge diagnosis of heart failure mean age 78 years the diagnosis was definite or probable in This would apply in very few cases below the age of 65, where a careful evaluation of any case of suspected heart failure would be mandatory.
Accordingly, it is unlikely that the strong association that we found would be due to misclassification of heart failure. A second limitation is the lack of information on subsequent weight development, and on other risk factors in adult life such as dyslipidaemia. A mildly elevated weight at the age of 18 years might be a marker of an increased risk of developing subsequent obesity.
A third limitation was that the findings of the present study are limited to Swedish men and may not be applicable to women or to other settings. The main strength of the present study is the uniquely large number of cases occurring at a young age. In conclusion, we found a steep increase in the risk of early heart failure associated with increasing body weight starting at levels that are considered normal. Given the global trend in adolescent overweight and obesity, early heart failure might well become a major threat worldwide, an aspect that has not received much attention in current prevention guidelines.
Supplementary material is available at European Heart Journal online. This work was supported by grants from: Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Close mobile search navigation Article navigation. Body weight in adolescence and long-term risk of early heart failure in adulthood among men in Sweden Annika Rosengren.
Heart failure , Adolescence , Hospital admission , Epidemiology. View large Download slide. Additionally adjusted for parental education, systolic and diastolic blood pressure. Additionally adjusted for IQ, muscle strength, and fitness. Population impact of heart failure and the most common forms of cancer: Heart failure in young adults: Shift in the composition of obesity in young adult men in Sweden over a third of a century.
Body mass index, abdominal fatness and heart failure incidence and mortality: Body weight in midlife and long-term risk of developing heart failure-a year follow-up of the primary prevention study in Gothenburg, Sweden. Young adulthood obesity and risk of acute coronary syndromes, stable angina pectoris, and congestive heart failure: Validity of an ergometer cycle test and measures of isometric muscle strength when prediction some aspects of military performance.
Cardiovascular and cognitive fitness at age 18 and risk of early-onset dementia. A simple method of determining confidence intervals for population attributable risk from complex surveys. Global, regional, and national prevalence of overweight and obesity in children and adults during — Alterations of left ventricular myocardial characteristics associated with obesity. Association of plasma free fatty acids and left ventricular diastolic function in patients with clinically severe obesity.
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Association of obesity in early adulthood and middle age with incipient left ventricular dysfunction and structural remodeling: Dramatic reversal of derangements in muscle metabolism and left ventricular function after bariatric surgery. We aimed to describe the time-dependent variation in high energy phosphate HEP metabolism of the two ventricles, and the relationship with endothelial activation and postoperative functional recovery. Fifty-two human donors had serial biopsies from the RV and the left ventricle LV at 1 initial evaluation, 2 after haemodynamic optimisation, 3 end of cold ischaemia, 4 end of warm ischaemia, 5 reperfusion, and 6 at 1 week postoperatively.
HEP was measured by chemiluminescence in biopsies 1—5 and adhesion molecules P-selectin, E-selectin, VCAM-1 and thrombomodulin were analysed by immunohistochemistry in biopsies 5—6. Seventeen donors and five recipients had RV intraoperative pressure—volume recordings by a conductance catheter. Six patients served as live controls. Brain death did not affect HEP metabolism quantitatively.
There was no difference between the RV and LV at any time point, but significant time-dependent changes were observed. Hearts with impaired function in the recipient showed marked variations in HEP levels at reperfusion, and those organs with RV dysfunction failed to replenish their energy stores. However, these organs were not different from normally functioning allografts in terms of endothelial activation and clinical risk factors. There was poor correlation between pressure—volume and HEP data in either donor or recipient studies.
Hearts followed-up with HEP and pressure—volume studies showed improvement in the recipient, despite functioning against a higher pulmonary vascular resistance. HEP are preserved over a wide range of contractile performance in the donor heart, with no metabolic difference between the two ventricles. No correlation with endothelial activation was seen either. Preservation efforts should be directed to the vulnerable periods of implantation and reperfusion.
Donor heart failure is the commonest cause of early mortality and an important cause of post-transplant morbidity [1] despite careful assessment of the organ prior to harvesting. While clearly multifactorial, the process of brain death significantly affects myocardial performance and experimental studies have shown that the right ventricle RV is affected more than the left ventricle LV.
The mechanism of this injury and its subsequent modulation by ischaemia and reperfusion are unknown, but it is clear that endothelial dysfunction of the allograft plays an important role [2 , 3]. Furthermore, previous studies by our group [4 , 5] and others [6] have shown that assessment of myocardial energy stores at the time of procurement is of value in predicting postoperative function.
The relationship between high energy phosphates HEP and myocardial function has not been examined, however, and the longitudinal changes that may occur throughout the early course of transplantation are unexplored. The purpose of this study was to describe the time course of HEP levels in both ventricles from the time of procurement to 1 week postoperatively and to examine coincident changes in myocardial performance and expression of surface antigens by the endothelium.
The effects of brain death per se were assessed by comparing these variables in hearts from brain-dead and non-brain-dead donors. Fifty-two donor hearts were studied. Six were considered unsuitable using our current organ selection criteria [7] and were not subjected to longitudinal assessment. In the remaining 46 hearts, serial biopsies were obtained at the following time points:.
The biopsies are named R1, L1, R2, L2, etc.
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Details of the patients are presented in Fig. Seventeen donors and five corresponding recipients also had an RV assessment with the conductance catheter.
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Local donors were haemodynamically optimised before biopsy 2 according to previously described protocols, in which the cornerstone of management was the use of the pulmonary artery catheter and hormone resuscitation. A potential limitation of our study is that eight donor hearts were retrieved by other centres. However, they were managed according to principles of donor optimisation and acceptance was based on our clinical criteria [7]. The donor heart was arrested with 1 l of St Thomas' 2 crystalloid solution and immersed in cold normal saline solution for transportation.
Where heart—lung blocks were retrieved pneumoplegia was preceded by a prostacyclin infusion directly into the pulmonary artery over 10—15 min details in Ref. Details of patients enrolled in the study.
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In 12 hearts procured by the Papworth team the initial biopsies 1 and 2 were not available because of lack of consent from the donor family. On 20 hearts, therefore, biopsies 1 and 2 were not available. The retrieval surgeon placed small purse strings on the anterior free wall of the RV and at the LV apex. The LV site was also used for venting and deairing after implantation. No complications related to this method of tissue sampling were recorded.
The 1-week biopsy was obtained in standard fashion via the transjugular route from the RV endomyocardium and processed for histology only. Forty-three transplants were performed and 42 cases were followed-up: The mean age of the heart recipients was The mean age of the heart—lung recipients was Topical cooling with cold saline was employed selectively depending on the surgeon's preference and modified reperfusion e. All patients had a central venous introducer and a pulmonary artery catheter was immediately floated whenever there was concern about allograft performance or to guide treatment of acute cardiac dysfunction.
Right heart failure was diagnosed if all the conditions below were satisfied: Immunosuppression consisted of triple therapy with steroids, cyclosporine and azathioprine. Trucut biopsies were immediately immersed in liquid nitrogen for storage. Neutralisation of the nucleotide mixture was carried out with a 0. Construction of a calibration curve with known amounts of adenine nucleotides was an initial obligatory step. Non-collagen protein was measured in each biopsy with a modification of the Bradford method, based on the dye-binding principle Bio-Rad, Hemel Hempstead, UK.
The average values for ATP and total adenine nucleotides of In 22 randomly selected sets of transplanted hearts formalin-fixed paraffin-embedded sections were stained for P-selectin, E-selectin, VCAM-1 and thrombomodulin. Appropriate positive controls were used and negative controls were performed by omission of the primary antibody.
Sections were initially stained with haematoxylin and eosin and examined for their general histological appearance. To ensure that the endothelium is intact even in the absence of ischaemic changes all biopsies were stained with CD31, a marker of histological integrity. CD31 was also used to count all the vessels on individual sections.
This assisted in evaluating P-selectin, the adhesion molecule with the highest expression in our study for a description of the principle see Tanio et al. Sections were examined by two independent observers blinded to the patient's identity and to the side and timing of the biopsy.
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For individual vessels excluding microcapillaries the staining for adhesion molecules was defined as present or absent. Results for adhesion molecules are reported as percentage of non-muscularised positive vessels. Thrombomodulin expression was scored on a scale of 0 absent to 5 normal, uniform staining. We described the time course of endothelial activation in clinical cardiac transplantation elsewhere [13]. In this study R5 and R6 biopsies only were compared for expression of endothelial markers in recipients with and without allograft failure Table 1.
RV functional assessment was carried out in 17 donors with stable circulation, once catecholamine support was minimised and loading optimised. A number of donor hearts were excluded from this component of the study by lack of consent from the recipient or by organ export to another centre. Recipient studies were carried out after separation from cardiopulmonary bypass in five selected heart transplants who were sufficiently stable for an invasive study. Recipients of heart—lung blocks were excluded due to the unknown variables introduced by the donor lungs at reperfusion. All studies were performed in the expiratory phase.
In essence, a 7Fr conductance catheter with incorporated solid-state pressure transducer Millar Instruments Inc. Pressure—volume loops were recorded at steady state, during parallel conductance determination, and during preload variation [14]. Preload variation was achieved by transient inferior venacaval snaring over at least five consecutive cardiac cycles. All results are averaged from at least two measurements.
The end-systolic presure—volume relationship ESPVR was produced by linear regression of consecutive systolic points in families of pressure—volume loops obtained during caval occlusion. The preload recruitable stroke work PRSW slope was calculated from a plot of stroke work against end-diastolic volume for these individual loops. Discrete variables were compared with Fisher's exact test.
To reduce bias from repeated measurements in the same patients, a mixed effects analysis of variance ANOVA was performed with stage as a fixed effect, and patient and repeated measures contrast as random effects. A P value of less than 0. A comparison was made between 23 hearts from brain-dead donors used for transplantation and six hearts from live patients three dominos and three controls undergoing aortic valve replacement.