Cooper Collection 076 (Change Of Heart)

A large number are hypertensive. It is important to take account of body surface area when measuring aortic size; these women are of small stature and the absolute aortic measurements may be normal. Women with existing cardiac disorders were possibly on a variety of medications prior to trying to become pregnant, and the decision to continue these medications during pregnancy is based on balancing the risk to the mother of stopping them, the availability of a safe alternative and the risk to the foetus.

Due to the ethical issue of performing clinical trials in pregnant women the only data on drugs in pregnancy are from observational studies and based on evidence from animal trials.

Whenever possible, prior to conception drugs considered to be unsafe during pregnancy should be stopped. However, many drugs need to be continued in pregnancy, and close liaison with foetal medicine specialists is important. Anti-coagulation is a source of problems in pregnancy. Where possible it should be substituted for low-molecular-weight heparin LMWH , which does not cross the placenta. However in the case of mechanical valves warfarin results in significantly less valve thrombosis than unfractionated heparin or LMWH [ 71 , 72 ].

If labour begins prematurely when the woman is still taking warfarin, a caesarean section must be performed. Currently there is no universally agreed upon strategy for the monitoring of enoxaparin use, with some centres using solely peak or trough levels of factor Xa, or both [ 77 ], and the strategy decided upon may be particularly important in the first trimester due to larger proportional changes in plasma volume and creatinine clearance [ 78 ]. The follow-up and delivery of high-risk pregnancy patients fitting into WHO class 3 [ 7 , 42 ] should occur in experienced centres where combined experienced anaesthetic, obstetric, cardiology and foetal care can be provided.

In many cases labour can be awaited naturally, although in some cases in which there is a desire to deliver early due to maternal complications, or for geographical reasons to allow for delivery in a specialist centre, induction of labour may be recommended. Caesarean section is associated with more profound and sudden haemodynamic changes, greater blood loss, increased risk of infection and dramatically increased risk of venous thromboembolism [ 80 ].

Furthermore, a Caesarean section will significantly affect the mode of future deliveries. However, it must be done in experienced hands by a specialist team. Caesarean section is reserved for obstetric indications; in rare cases, if there is a very high risk of aortic dissection, a planned delivery in theatres with a cardiac surgeon on stand-by is recommended. The third stage of labour is usually facilitated by the administration of syntometrine, which causes uterine contractions and minimises post-partum haemorrhage. However, this drug also has a pronounced hypertensive and vasoconstrictive effect and so is avoided in most women with heart disease in favour of a slow infusion of syntocinon an oxytocin analogue [ 82 ].

Misoprostol may be used for post-partum haemorrhage, with syntometrine reserved only for severe maternal haemorrhage where the benefit outweighs the risk [ 82 ]. Whilst pre-pregnancy assessment and surveillance during pregnancy are very important, post-partum follow-up is also important to assess for deterioration following pregnancy [ 20 ] and to monitor for peripartum cardiomyopathy, which can occur late in the post-partum period. Some conditions, such as long QT and Marfan syndrome, seem to be associated with more complications in the post-partum period, and advising women accordingly is important prior to discharge.

Post-partum follow-up also allows for the reintroduction of important cardiac medications whose use may have been altered during pregnancy, such as angiotensin-converting enzyme inhibitors or warfarin. Post-partum is a key opportunity to discuss contraception and the options available to women to reduce the risk of an unplanned pregnancy, as well as to allow recovery from the most recent pregnancy, especially in the context of peripartum cardiomyopathy.

Pregnancy presents the heart with a unique physiological challenge. An increasing number of women with cardiac disease are going through pregnancy successfully. The range of conditions encountered is wide, and many patients have congenital heart disease. There are multiple management challenges to achieve a successful outcome for mother and child. Pre-pregnancy counselling is vital, and specialist multi-disciplinary care by a specialist team is essential to ensure a successful outcome for mother and child. No funding or sponsorship was received for this study or publication of this article.

All named authors meet the International Committee of Medical Journal Editors ICMJE criteria for authorship for this manuscript, take responsibility for the integrity of the work and have given final approval for the version to be published. To view enhanced content for this article go to http: National Center for Biotechnology Information , U.

Journal List Cardiol Ther v.

1. The Seeds of the Storm (The Song of the Ferryman Book 1)!
2. LIBRO XIX DE POESÍAS ANDALUZAS: (POESÍA ANDALUZA ACTUAL nº 19) (Spanish Edition);
3. Making The Best Of A Dysfunctional Relationship : Mending The Bond - Creating A Healthy Relationship.
4. Methods and statistics.

Published online Jul 5. Reza Ashrafi and Stephanie L. Author information Article notes Copyright and License information Disclaimer. Received Feb Abstract Cardiac disease remains a major cause of morbidity and mortality in pregnant and post-partum women, although progress has been made, with specialist joint obstetric—cardiology clinics providing an integrated, safe and personalised service to these women.

Pregnancy, Heart disease, Gender. Introduction With improved maternal medical care and fertility treatments, an increasing proportion of women with congenital cardiac disease and acquired heart disease are becoming pregnant and delivering safely [ 1 ]. Physiological Changes in Pregnancy Pregnancy has a dramatic effect on the cardiovascular system, and the effects are sustained into the post-partum period. Open in a separate window.

Pre-conception Management In this section we discuss those aspects of cardiac—pregnancy management which most physicians feel to be of the greatest importance, and the identification of women at risk and their pre-pregnancy counselling of their own individual risk involved in pregnancy and delivery. Pre-pregnancy Counselling and Risk Assessment The most important aspect of assessment of reproductive-age women with cardiac disease is pre-conception counselling. Termination should be discussed. Pregnancy and Pre-delivery After the key phase of pre-assessment, and care focusses on the assessment during pregnancy and the management of specific conditions.

Clinical Assessment and Investigations During Pregnancy Cardiac assessment of the pregnant patient can be difficult as common symptoms of pregnancy, such as breathlessness and fatigue, can mimic cardiac symptoms. Common and Important Cardiovascular Disorders Encountered During Pregnancy Specific guidance on some of the more commonly encountered conditions and important high-risk conditions are discussed in this section.

Arrhythmias 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. Congenital Heart Disease In developed countries, most women seen in cardiac—obstetric clinics have congenital heart disease [ 67 ]. Aortopathies 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.

Management of Pharmacological Treatment in Pregnancy and Post-partum Women with existing cardiac disorders were possibly on a variety of medications prior to trying to become pregnant, and the decision to continue these medications during pregnancy is based on balancing the risk to the mother of stopping them, the availability of a safe alternative and the risk to the foetus.

1. Anyone Can Write.
2. Anyone You Want Me To Be: A Shocking True Story of Sex and Death on the Internet.
3. Introduction;
4. .

Management of Labour and Delivery in Women with Cardiovascular Disorders The follow-up and delivery of high-risk pregnancy patients fitting into WHO class 3 [ 7 , 42 ] should occur in experienced centres where combined experienced anaesthetic, obstetric, cardiology and foetal care can be provided. Post-partum Evaluation and Management of Women with Cardiovascular Disorders Whilst pre-pregnancy assessment and surveillance during pregnancy are very important, post-partum follow-up is also important to assess for deterioration following pregnancy [ 20 ] and to monitor for peripartum cardiomyopathy, which can occur late in the post-partum period.

Conclusion Pregnancy presents the heart with a unique physiological challenge. Acknowledgements No funding or sponsorship was received for this study or publication of this article. Compliance with Ethics Guidelines This article does not contain any new studies with human or animal subjects performed by any of the authors. Footnotes Enhanced content To view enhanced content for this article go to http: Medical and obstetric outcomes among pregnant women with congenital heart disease. ESC Guidelines on the management of cardiovascular diseases during pregnancy. The task force on the management of cardiovascular diseases during pregnancy of the european society of cardiology ESC Eur Heart J.

Incidence and causes of maternal mortality in the USA. J Obstet Gynaecol Res. Incidence and prevalence of pregnancy-related heart disease. The worldwide epidemiology of acute rheumatic fever and rheumatic heart disease. Reviewing maternal deaths to make motherhood safer: Cardiac output and related haemodynamics during pregnancy: Nitric oxide and pregnancy.

Cardiovascular magnetic resonance in pregnancy: J Cardiovasc Magn Reson. A longitudinal study of maternal cardiovascular function from preconception to the postpartum period. Serial study of factors influencing changes in cardiac output during human pregnancy. Hunter S, Robson SC. Adaptation of the maternal heart in pregnancy. Arterial dissections associated with pregnancy.

Pregnancy in patients with pre-existing cardiomyopathies. J Am Coll Cardiol. Long-term outcome following pregnancy in women with a systemic right ventricle: Assisted reproductive technology and pregnancy-related hypertensive complications: Pregnancy-related complications and adverse pregnancy outcomes in multiple pregnancies resulting from assisted reproductive technology: Maternal folic acid supplementation and the risk of congenital heart defects in offspring: Prenatal multivitamin supplementation and rates of congenital anomalies: J Obstet Gynaecol Can. Cardiac disease in pregnancy I: Predictors of pregnancy complications in women with congenital heart disease.

Risks of contraception and pregnancy in heart disease. Pregnancy and delivery in cardiac disease. Emmanuel Y, Thorne SA. Heart disease in pregnancy. Electrocradiographic Qrs Axis, Q wave and T-wave changes in 2nd and 3rd trimester of normal pregnancy. J Clin Diagn Res. Doctor, will that x-ray harm my unborn child? Structural and functional changes in maternal left ventricle during pregnancy: Maternal left ventricular diastolic and systolic long-axis function during normal pregnancy.

Morphological and functional adaptation of the maternal heart during pregnancy. Altered maternal left ventricular contractility and function during normal pregnancy. It would be particularly helpful for the operating surgeon to have a test which is predictive of donor organ failure, such that prophylactic treatments e. Until such an instrument is available caution should be exercised so as to avoid an accumulation of clinical risk factors in individual cases. Given the increased inflammatory load of the donor heart in general, it was interesting to see that endothelial activation was not different either between the two groups Table 1.

Biopsies 5 and 6 are, however, snapshots in what is thought to be an intricate process of endothelial modulation post-reperfusion. This area requires further investigation. Perhaps donor organ failure, whether temporary or fatal, results from a more complex combination of intrinsic contractile dysfunction and variable loading conditions, particularly in the pulmonary bed. Finally, although marked variations in HEP levels at reperfusion may challenge the robustness of this assessment method, it is reassuring that other groups noticed the same phenomenon see discussion in Ref.

With the variables studied, a dissociation between energy metabolism and contractile function was demonstrated in the human donor heart. HEP levels in brain-dead donors did not correlate with the cardiac index measured by thermodilution or with RV load-independent parameters.

Electrocardiography - Wikipedia

All biochemical and haemodynamic parameters improved after reperfusion, but only three of the variables were in the range of statistical significance Table 3. This improvement took place despite implanting the heart in a circulation with a much higher pulmonary vascular resistance Since none of the five patients developed donor organ failure, perhaps removal of the heart from the brain-death environment was sufficient to ensure better function in these cases.

This is a cautious conclusion based on small numbers. Some of the observed improvement may actually be due to the regular low dose of inotropic treatment used in three of the recipients at the time of recording. Other groups analysed the metabolic state of the donor heart using 31 P magnetic resonance spectroscopy [22]. A correlation was found between the energy content expressed as creatine phosphate to ATP ratio and the cardiac index at 1 week postoperatively, but not in the early postoperative period.

Spectroscopic methods are in addition limited in their ability to be repeated in the intraoperative period. In a more general context, there is ongoing debate in areas of experimental and clinical cardiology on the relationship between HEP levels and contractile function [23—26]. The weight of evidence suggests that HEP levels are preserved over a wide range before systolic function is affected. In practical terms, as we have seen in this study, normal levels of adenine nucleotides in the cardiac tissue do not exclude early clinical dysfunction.

In fact they tell us little about possible perturbations in ATP turnover or utilisation by the contractile apparatus. Recent studies show that HEP do not diffuse through the cytoplasm in homogenous fashion. On the contrary, the myocardial sarcoplasm is a sum of microdomains with restricted diffusion and preferential channelling of substrates to enzymes [27]. The efficiency of ATP utilisation is beyond the possibilities of current research.

Taken together, these results suggest that the fate of the HEP adenine nucleotides at reperfusion remains incompletely described in transplantation, particularly in relation to clinical outcomes. Transplant surgeons would much appreciate a marker of intrinsic donor heart function, especially for borderline organs. In clinical studies reporting outcomes of donor hearts, a non-quantifiable variable is the amount of brain death-induced cardiac dysfunction. Earlier work from the Papworth group showed that hearts with an impaired birefringence index a laboratory measure of biochemical and contractile function have poor early and late clinical outcome [4].

These observations were made before introducing routine instrumentation of all donor hearts with a pulmonary flotation catheter in Some may have been turned down by current Swan—Ganz catheter criteria [7] , which could explain the magnitude of the initial birefringence observations. Our current study group contained six patients whose hearts were turned down from donation and only two of those were rejected on functional grounds.

1 Introduction

We feel that any donor hearts excluded from donation by structural disease e. With such a small number of observations it is impossible to judge how good HEP levels are at detecting unsuitable organs. The two poorly functioning hearts were also failing on conventional Swan—Ganz haemodynamic criteria and on the basis of inotropic load too. This suggests that HEP levels may become a sensitive marker of cardiac function only when the heart is failing clinically, despite resuscitative efforts. This notion is in agreement with recent experimental reports, in which the reduced afterload and coronary perfusion were shown to be critically involved in brain death-induced cardiac dysfunction [28].

From the clinicians standpoint this implies that, within the practice of donor optimisation, a finer index of intrinsic cardiac function will have to be identified. Although HEP have been a critical endpoint in myocardial protection research, the cumulative injury sustained in transplantation and the observed variability in HEP levels make this tool appropriate for research purposes only. In summary, we have shown that the energy metabolism of the two ventricles evolves in parallel across transplantation. There appears to be no immediate relationship between energy stores, endothelial activation and contractile function.

The most vulnerable periods appear to be warm ischaemia and reperfusion and this is perhaps where most preservation efforts should be directed in future studies. Dr Darracott-Cankovic kindly provided us with previously unpublished observations. Murday Glasgow, United Kingdom: Could you comment on strategies to improve that circumstance, in other words, to improve the high-energy phosphate load after reperfusion, for example, substrate-enhanced reperfusion during that time.

There is a multitude of strategies, and my view is that every little helps. There has been, for example, a study of donor blood cardioplegia from Italy and that showed a reduction in the incidence of right ventricular failure post transplant. Another randomized study from Montreal showed that modifying reperfusion is also beneficial.

This can be done with leukocyte filters, Trasylol, hotshots, substrate enhancement, as you suggested. But the number of randomized clinical experiments in this area is actually very small, so there's a lot of work to be done. Did you see any effect of the cause of brain deaths on energy loads? Or maybe the patient committing suicide is different from a patient dying from a cerebrovascular event with the history of hypertension. Did you see any effect of the underlying cause of brain death? We did not look at that particular issue.

And I know there is some evidence to suggest that the cause of brain death has an impact on recipient outcome. We hold the view that whatever the cause of brain death, the physiological derangement can be so profound, and the subsequent injury with ischemia and reperfusion is so complex, that analyzing this variable in isolation doesn't take us any further. And we never like to say that we rule out a brain death donor from head trauma on these grounds alone. Stoica, I think in that context it is very important to answer the question whether all these patients underwent your specific pre-explant protocol?

Because I think that's the most important probably, that you start from a relatively, let's say, stable level. And though the differences between the events prior to that might be less than in other collectives and other cohorts. Do you agree or not? Well, that's certainly possible. But this physiological study describes what happens in an average set of hearts subjected to our protocol of optimization. So it's difficult for me to speculate on the particular cause of brain death.

• Heart Disease and Pregnancy?
• ?
• !
• .
• How Any Man Can Become a Guru of Dating- Simple, Easy & Great Dating Tips Collection;
• .

I don't know the answer to that. 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. Cardiac - physiology Subject: Close mobile search navigation Article navigation. The energy metabolism in the right and left ventricles of human donor hearts across transplantation Serban C.

Heart transplantation , Brain death , Endothelium , Energy stores , Myocardial contractility.



View large Download slide. The registry of the international society for heart and lung transplantation: Can perioperative high-energy phosphate analysis aid the assessment of donor heart viability? Adenine nucleotide catabolism in human myocardium during heart and heart—lung transplantation. Swan—Ganz catheter assessment of donor hearts: The contribution of donor management and modified cold blood lung perfusate to post-transplant lung function. Simple assay of 0. Patients remained in the study if they were unable or unwilling to undergo recommended specific tests. Cardiac MRI was analyzed by an expert and assessed for evidence of ARVC, sarcoidosis, myocarditis, unrecognized myocardial infarction or other explanatory causes.

In a population of a variety of cardiovascular disorders, PVCs were found to range from per hour , but have also been recorded in healthy individuals , , so this study used a conservative amount when identifying an abnormal number of PVCs. Electrophysiological EP testing was performed at the investigators discretion, using standard protocols that permit up to 3 ventricular extra stimuli at 2 drive cycle lengths for induction of ventricular arrhythmias Electro-anatomical mapping was performed in select cases where ARVC was suspected.

Exercise stress tests were performed using a Bruce or modified Bruce protocol. Patients underwent a lead ECG while in a supine position, immediately when standing, and continuously during treadmill exercise testing Investigators were asked to review the entire patient record including the nature and context of symptoms, family history, and results of clinical and genetic testing and render a working diagnosis, with a qualitative descriptor of the strength of the diagnosis ie.

For the purpose of classification and comparison, patients were divided into two groups; diagnosed based on a definite or probable diagnosis, and undiagnosed based on unexplained cardiac arrest or only weak evidence of a diagnosis possible diagnosis, single inconclusive test Table 8: Testing was accessed on the basis of clinical testing from commercial vendors.

Prior to access to clinical genetic testing in , limited research testing assessed 7 patients. Genomic DNA was isolated from blood lymphocytes and screened with direct sequencing performed on suspected culprit genes. ATP was only included when it was responsible for termination of the ventricular tachycardia as ATP may also occur during charging of the ICD prior to shock. Patients required a minimum of 12 months follow-up to ensure sufficient time for events to occur. Outcome ascertainment was not blinded to the patients clinical history or working diagnosis.

SCIVF patients were treated as diagnosed due to recent studies suggesting the benefit of quinidine in this population Cox regression models were also constructed for those with a diagnosis, comparing time to first event and hazard ratios in patients with a structural diagnosis, to those with an electrical diagnosis. These models were adjusted for age and sex of the patients. Statistical analysis was performed to determine if any factors were predictive of future events.

Lastly, genetics was included in the model, where genetics was reported as normal, variant of unknown significance, or pathogenic. A Spearman correlation was used to determine whether any of the testing was correlated with future events. Models using linear regression were also constructed, aiding to determine whether any group of diagnostic testing was predictive of future events.

Results A total of patients were enrolled between January 1, and December 1, from 14 sites across Canada Table 9. Patients had a mean age of Patient Demographics and Diagnostic Information. Eight probands had a change in their diagnosis during follow-up as more information became available. Some tests were repeated during follow-up or when results were borderline, resulting in each patient undergoing 8. Table 11 shows complete results of all the clinical testing. Summary of Total Numbers of Clinical Testing Further investigation was performed, targeting diseases where multiple clinical tests may contribute to the diagnosis.

The other BrS patient had a borderline procainamide, but with genetic testing was found to be a carrier of a pathogenic SCN5A mutation. Sensitivity and Specificity of Clinical Testing Sensitivity and Specificity of testing, compared to definite or probable diagnosis 60 Figure The mean duration of follow-up was 3. Symptoms at follow-up, including palpitations, syncope, and deaths were ascertained during follow-up, detailed in Table Two patients died during follow-up, one with a diagnosis of sarcoidosis who died of VT storm due to lead failure and the inability to deliver high voltage therapy.

This patient was originally diagnosed with ARVC, but sarcoidosis was discovered at autopsy, allowing for the diagnosis of a first-degree family member with rare familial sarcoidosis. The second patient that died was diagnosed with LQTS and eventually died from malignancy. Follow-up Events, Comparing Patients with and without a Diagnosis. Survival models were constructed using Cox regression analysis to compare the time to first ICD shock, time to first ATP, and time to first event shock or ATP in patients with and without a diagnosis Figure Unadjusted and adjusted age and sex hazard ratios were calculated and are listed in Figure 17 and Table Time to First event, Comparing Patients with and without Diagnosis.

Adjusted and Non-adjusted Hazard Ratios For patients with a diagnosis, comparisons were made between those with underlying structural heart disease and those with primary electrical disease Table In follow-up, there was no difference in symptoms between these two groups Table Analysis was performed to determine if there was a correlation between positive clinical testing and future cardiac events, or if positive clinical testing was predictive of future events.

Spearman correlation and linear regression modeling was performed with neither having any significant results Appendix. Discussion The current study has shown that with systematic advanced testing, a clinical diagnosis can be determined in approximately half of patients presenting with an unexplained cardiac arrest.

A variety of diagnostic testing techniques are required as the unexplained cardiac arrest patients make up an eclectic group of diagnoses, which includes both primary electrical diseases and latent structural causes. CASPER excluded patients with coronary artery disease, the most frequent cause of cardiac arrest 5 , and overt structural heart disease, so it would be expected that more patients would have primary electrical disease as the culprit of the cardiac arrest.

Patients that were diagnosed subsequently were offered family screening to identify additional relatives at risk of a cardiac arrest. As has been previously reported , many of the diseases identified in CASPER are diverse, dynamic and have overlapping phenotypes. Seven percent of patients were diagnosed during follow-up, as phenotypes became more evident or more information became available about the underlying disease.

Furthermore, eight patients had a change in their diagnosis, due to overlapping phenotypes or borderline clinical testing. These results highlight the importance of continuous follow-up and monitoring of patients as phenotypes may become more evident, or more information may become available to allow for diagnosis, and subsequent refined treatment options and family screening. Since the initiation of CASPER in , continued research has led to the acceptance of new mechanisms responsible for cardiac arrest, including short-coupled IVF and early repolarization , , It is not known to be familial, which warrants further study to determine mechanisms.

The SCIVF diagnosis could only be made in patients being monitored at the time of the VF, either through telemetry or during follow-up events recorded by their ICD, so the diagnosis required a second cardiac event after the index event while the patient was being monitored. This will require continuous monitoring for secondary events to gain a clearer picture of its prevalence. Full results may be found in a previously published study , however the study by Derval et al.

For purposes of strict definition, patients in the current analysis received a diagnosis of early repolarization if it was the only known reason for the cardiac arrest. As previously stated, coronary artery disease is the most likely culprit for cardiac arrest, and CAD should be ruled out for all patients presenting with a cardiac arrest. Once structural heart disease has been ruled out, investigators should direct their attention to the diagnosis of primary electrical diseases. Our previous reports regarding epinephrine challenge raised concern that specificity may be a concern, in contrast to procainamide infusion 51, Both tests appear to be appropriate with a modest yield, but require contextual interpretation because of inherent limitations in reproducing specific pathogenic findings.

If the cardiac arrest occurred during rest, the patient should undergo a procainamide infusion, as it was the best test for diagnosing Brugada Syndrome. Despite a high rate of positive testing, the EP testing should be used as a last resort as the EP testing was responsible for a diagnosis in only one patient with ARVC, and is 70 invasive.

Based on the evidence from this study, a diagnostic pathway has been proposed in Figure Genetic testing should be performed to confirm a diagnosis and used to identify family members who may be susceptible to future cardiac events due to IHRD. Proposed Diagnostic Pathway The ICD intervention rate in the current study was higher than anticipated in a cohort with preserved cardiac function and a latent substrate for cardiac arrest. We were unable to detect a difference in event rate between those with a diagnosis to those without a diagnosis, including time to first ICD shock, time to first ATP and time to first event shock or ATP.

ProcainamideUCA during exercise or stress? Conceptually, this may be related to disease severity, but given that the comparator by definition has unexplained cardiac arrest, mechanistic explanations cannot be explored unless a cause becomes evident. Future studies may demonstrate that the ability to diagnose patients is a form of risk stratification for future events. The current study has not yet accrued sufficient follow-up to determine if these trends are real and have diagnostic or therapeutic implications. Previous studies have reported that those with a previous cardiac arrest due to VF are at a higher risk of second events, but results from studies investigating follow-up ICD events in unexplained cardiac arrest patients have been mixed , , Conclusion This study represents a rare cohort of individuals who have suffered an unexplained cardiac arrest, and represents the largest cohort studied to date.

Overall, this study shows that with advanced testing, investigators are able to determine a diagnosis in approximately half of previously unexplained cardiac arrest patients. Over two-thirds of the patients had a potentially inherited mechanism of disease, allowing for family screening and identifying those at risk of a cardiac arrest. Continued monitoring is imperative as these primary electrical diseases or latent structural causes are often dynamic and phenotypes may become more evident with repeated testing, or recording of events that lead to a diagnosis.

Furthermore, results from this study highlight the potential for diagnosis to aid in risk stratification to determine those whom are more likely to have a future cardiac event. This study also provides physicians with strategies for identifying underlying conditions, and provides annual shock rates to communicate to patients, and to develop strategies to mitigate shock risk. As is expected with rare diseases, our cohort is relatively small, making reporting on the ICD event rate difficult with few actual events. An increase in follow-up and more ICD events rates may provide insight into annual shock rates and allow for the determination of clinical tests that may be predictive of future events.

Furthermore, patients included in this study represent the patients who have survived a cardiac arrest, and results from this study may not be applicable to non-survivors of a cardiac arrest, unexplained after an autopsy report. Procainamide was the only sodium channel blocker used for the detection of Brugada syndrome, as it is the only sodium channel blocker available in Canada.

Future directions of this study are to continue to monitor the patients enrolled, and to continue to enroll other patients to increase the cohort and subsequent number of cardiac events. Furthermore, we recently received a grant from the Rare Disease Foundation to conduct a study on ICD programming in this cohort.

We aim to determine whether there is a comparable benefit in those without coronary artery disease or underlying reduced heart function dilated cardiomyopathy , who undergo ICD implantation for secondary prevention due to a previous unexplained cardiac arrest. Lastly, a future goal is to conduct research to better understand environmental risks that may be associated with increased risks in cardiovascular events in patients with previous UCA.

Electrocardiography

For example, in , the American Heart Association stated that short-term increase in air pollution may have lead to the early mortality of thousands of individuals in the United States alone, by methods which may include QT interval prolongation due to intraventricular conduction delay Diesel exhaust is a major source of traffic-related air pollution and has been shown to cause vasoconstriction of blood vessels in human subjects, but no studies have studied the effect of diesel exhaust on repolarization Furthermore, while the effects of air 74 pollution on cardiovascular disease are concerning, the evidence has mostly relied on epidemiological studies and have involved healthy populations , Few studies have completed randomized control trials in high-risk populations.

A future goal is to conduct a randomized control trial comparing UCA patients to normal, healthy volunteers, to determine whether UCA patients are at a high risk for cardiac events due to air pollution, and whether recommendations should be made regarding occupation and location of residence. Life threatening causes of syncope: Mortality, summary list of causes The Canadian Heart Health Strategy: Ilkhanoff L, Goldberger JJ. Association of national initiatives to improve cardiac arrest management with rates of bystander intervention and patient survival after out-of-hospital cardiac arrest.

Risk stratification for arrhythmic sudden cardiac death: Predictors of survival from out-of-hospital cardiac arrest: Circulation Cardiovascular quality and outcomes. Sudden Cardiac Death in the United States, to Sports-related sudden death in the general population. Sudden death in young athletes. The New England journal of medicine. Diagnostic yield in sudden unexplained death and aborted cardiac arrest in the young: Unfavorable outcome in patients with primary electrical disease who survived an episode of ventricular fibrillation.

Viskin S, Belhassen B. Sudden cardiac arrest in the young due to inherited arrhythmias: Pacing and clinical electrophysiology: Abnormal electrocardiographic findings in athletes: British journal of sports medicine. Inherited heart rhythm disease: The Canadian journal of cardiology.

Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome: Journal of the American College of Cardiology. Refugee stress and folk belief: Pathogenesis of sudden unexplained nocturnal death lai tai and endemic distal renal tubular acidosis. The enigma of "bangungut". A pathological study on sudden and unexpected death, especially on the cardiac death autopsied by medical examiners in Tokyo. General anxiety, depression, and physical health in relation to symptoms of heart-focused anxiety- a cross sectional study among patients living with the risk of serious arrhythmias and sudden cardiac death.

Health and quality of life outcomes. A new management of syncope: The Fainting Assessment Study. Journal of cardiovascular electrophysiology. Transient loss of consciousness and syncope. Handbook of clinical neurology. Incidence and Prognosis of Syncope. New England Journal of Medicine. Standardized human pedigree nomenclature: Journal of genetic counseling.

Rapid Interpretation of EKG's. Inherited Heart Rhythm Disease: Negotiating the Minefield for the Practicing Cardiologist. Canadian Journal of Cardiology. Use of signals in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction. Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts. Effect of change in posture and exercise on repolarization in patients with long QT syndrome with HERG channel mutations.

Utility of treadmill testing in identification and genotype prediction in long-QT syndrome. Circulation Arrhythmia and electrophysiology. The American journal of cardiology. An analyisis of time relations of electrocardiograms. Comparison of automatic QT measurement techniques in the normal 12 lead electrocardiogram. Accurate electrocardiographic assessment of the QT interval: Epinephrine-induced QT interval prolongation: Epinephrine-induced T-wave notching in congenital long QT syndrome.

Epinephrine QT stress testing in the evaluation of congenital long-QT syndrome: Diagnosis of unexplained cardiac arrest: Arrhythmia characterization and long-term outcomes in catecholaminergic polymorphic ventricular tachycardia. The relationship between plasma concentration of metoprolol and CYP2D6 genotype in patients with ischemic heart disease. Procainamide infusion in the evaluation of unexplained cardiac arrest: Effects of isoproterenol and propranolol on the inducibility and frequency of ventricular fibrillation in patients with Brugada syndrome.

Handbook of Cardiac Electrophysiology: Sensitivity and Specificity of Substrate Mapping: Gepstein L, Evans SJ. Electroanatomical mapping of the heart: Limits of normal left ventricular dimensions in growth and development: J Am Coll Cardiol. Usefulness of echocardiography in preparticipation screening of competitive athletes. Revista espanola de cardiologia English ed.

Classification of the cardiomyopathies: Implantable cardioverter defibrillators for the treatment of arrhythmias and cardiac resynchronisation therapy for the treatment of heart failure: Health technology assessment Winchester, England.

Heart Disease and Pregnancy

Survival of the fittest: Characterization of left ventricular diastolic function by tissue Doppler imaging and clinical status in children with hypertrophic cardiomyopathy. The international journal of cardiovascular imaging. Late gadolinium enhancement among survivors of sudden cardiac arrest.

Goldman L SA, editor. Quantification of coronary artery calcium using ultrafast computed tomography. Clinical profile and long-term follow-up of 37 families with arrhythmogenic right ventricular cardiomyopathy. Prevalence of right ventricular dysplasia-cardiomyopathy in a non-referral hospital. Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening program. Arrhythmogenic Right Ventricular Cardiomyopathy. Genetics of Right Ventricular Cardiomyopathy.

American journal of medical genetics Part C, Seminars in medical genetics. Proposed Modification of the Task Force Criteria.