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Can artificial intelligence save our lives?

The role of artificial intelligence (AI) in our life is advancing rapidly and is making strides in early detection of diseases. The consumer market is composed of wearable health devices that enables continuous ambulatory monitoring of vital signs during daily life (at rest or physical activity), or in a clinical environment with the advantage of minimizing interference with normal human activities1. These devices can record a wide spectrum of vital signs including: heart rate and rhythm, blood pressure, respiratory rate, blood oxygen saturation, blood glucose, skin perspiration, body temperature, in addition to motion evaluation. However, there is a lot of controversy whether these health devices are reliable and secure tools for early detection of arrhythmia in the general population2.

Atrial fibrillation (afib) is the most common arrhythmia currently affecting over 5 million individuals in the US and it’s expected to reach almost 15 million people by 2050. Afib is associated with an increased risk of stroke, heart failure, mortality and represents a growing economic burden3. Afib represents a diagnostic challenge, it is often asymptomatic and is often diagnosed when a stroke occurs. Afib represents also a long term challenge and often involves hospitalization for cardioversion, cardiac ablation, trans-esophageal echo, anti-arrhythmic treatment, and permanent pacemaker placement. However, if afib is detected, the risk of stroke can be reduced by 75% with proper medical management and treatment3.

Physicians need fast and accurate technologies to detect cardiac events and assess the efficacy of treatment. A reliable, convenient and cost-effective tool for non-invasive afib detection is desirable. Several studies assessed the efficacy and feasibility of wearable technologies in detecting arrhythmias. The Cleveland clinic conducted a clinical research where 50 healthy volunteers were enrolled. They tested 5 different wearable heart rate monitors including: (Apple Watch, Garmin Forerunner, TomTom Spark Cardio, and a chest monitor) across different types and intensities of exercises (treadmill, stationary bike and elliptical). The study found that chest strap monitor was the most accurate in tracking the heart rate across different types and intensities of exercises4.

The Apple and Stanford’s apple Heart Study enrolled more than 419,297 Apple Watch and iPhone owners. Among these users 2,161 (roughly 0.5%) received a notification of an irregular pulse. Of those who received the notifications, only about 450 participants scheduled a telemedicine consultation and returned a BioTelemetry ECG monitoring patch. When the Apple Watch notification and ECG patch were compared simultaneously, researchers found 71% positive predictive value and about 84% of the cases were experiencing Afib at the time of the alert. Additionally, in 34% of participants whose initial notification prompted an ECG patch delivery were later diagnosed with Afib. This finding shows that Apple watch detected afib in about one third of the cases which is “good” for a screening tool considering the “intermittent nature of afib and that it may not occur for a whole week” says Dr. Christopher Granger, a professor of medicine at Duke University who participated on the steering committee for the Apple Heart study5.

These studies are observational studies and are not outcome driven. They are not randomized and are not placebo controlled. There are potentials for false negatives, where the Apple watch fails to detect the afib and false positive where it detects arrhythmia that does not exist. Unfortunately, patients who are false negative don’t consult the physician about their symptoms of palpitations and shortness of breath since it provides false security. While patients with false positive are sent unnecessarily to the clinic that could lead to further unnecessarily test and anxiety for the patient.

Is the Apple Watch ready to be used as a default screening tool to monitor the heart rate and rhythm in the general population and by physicians with patients with or at high risk for Afib is still unclear and warrant further studies.  In conclusion, physicians should be cautious when using data from consumer devices to treat and diagnose patients.

 

References:

  1. Cheung, Christopher C., Krahn, Andrew D., Andrade, Jason G. The Emerging Role of Wearable Technologies in Detection of Arrhythmia. Canadian Journal of Cardiology. 2018;34(8):1083-1087. doi:10.1016/j.cjca.2018.05.003
  2. Dias D, Paulo Silva Cunha J. Wearable Health Devices-Vital Sign Monitoring, Systems and Technologies. Sensors (Basel). 2018;18(8):2414. Published 2018 Jul 25. doi:10.3390/s18082414
  3. Chugh, S., Sumeet, Havmoeller, J., Rasmus, Narayanan, F., Kumar, et al. Worldwide Epidemiology of Atrial Fibrillation: A Global Burden of Disease 2010 Study. Circulation. 2014;129(8):837-847. doi:10.1161/CIRCULATIONAHA.113.005119
  4. Wrist-Worn Heart Rate Monitors Less Accurate Than Standard Chest Strap. Medical Design Technology. http://search.proquest.com/docview/1875621494/. Published March 9, 2017.
  5. Turakhia, Mintu P., Desai, Manisha, Hedlin, Haley, et al. Rationale and design of a large-scale, app-based study to identify cardiac arrhythmias using a smartwatch: The Apple Heart Study. American Heart Journal. 2019;207:66-75. doi:10.1016/j.ahj.2018.09.002

 

 

The views, opinions and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your personal health matters. If you think you are having a heart attack, stroke or another emergency, please call 911 immediately.

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The 21-year-old man who survived an acute myocardial infarction

One of the most important things we can do as health-care providers, parents, teachers, caregivers and peers is to successfully recognize and improve the health issues and health outcomes of the teens and young adults. In this blog I’ll share the story of a young man who was seen by my husband in the ED and sparked my interest as a scientist to study the prevalence and clinical profile of myocardial infarction (MI) in young adults in my community.

I encourage you to share this blog with the young adults in your life, as well as parents and caregivers who have teenagers:

Three nights ago as my husband was preparing to sign off his shift in the ED, a 21 years-old man was brought in by the ambulance with a 30-minute history of severe central, crushing pain radiating down to his left arm. The pain was associated with nausea, vomiting, sweating and breathlessness. It was his first time to ever experience a central crushing pain. The man had a history of membranoproliferative glomerulonephritis and was on immunosuppressive therapy. He was also diagnosed with secondary hypertension and was on enalapril and nifedipine. Thankfully, he was in safe hands, the ED team were able to recognize his symptoms and a diagnosis of acute myocardial infarction was made. But, can you imagine how emotionally and physically upsetting this was to himself and his family.

Overview

Coronary artery disease (CAD) is the leading cause of morbidity and mortality worldwide. Myocardial Infarction (MI) is a lethal manifestation of CAD and can present as sudden death. Although it mainly occurs in patients older than 45 years, young men and women can suffer from myocardial infarction1. Unfortunately, when it happens to young adults, the disease can carry significant psychological impact, financial constraints and morbidity to the patients and their family. The protection being offered by young age is gradually being taken away with the high prevalence of CAD risk factors in these young adults such as obesity, lack of physical activity and smoking. Several studies have described the clinical profile and outcome of young patients with MI and its incidence ranged between 2%-10%. Overall, young patients are more likely to be male, with a history of smoking and hyperlipidemia, however, they were less likely to have other comorbidities and less extensive CAD on coronary angiogram2.

Causes of myocardial infarction in young adults

The causes of myocardial infarction in young adults can be broadly divided into two groups, those with angiographically normal coronary arteries and those with coronary artery disease of varying etiology.

Angiographically “normal” coronary arteries

  • Hypercoagulable state:
    • Nephrotic Syndrome
      • Proteinuria associated with the nephrotic syndrome results in the loss of low molecular weight proteins which alters the concentration and activity of coagulation factors. As a result, factors IX, XI and XII are decreased due to urinary excretion. While the liver tries to compensate for the hypoalbuminaemic state, there is an increased synthesis of factor II, VII, VIII, X, XIII and fibrinogen resulting in raised blood levels3.
    • Antiphospholipid syndrome (Hughes syndrome)
      • Arterial and venous thrombosis is a prominent feature of this syndrome together with antiphospholipid antibodies and miscarriage in pregnancy. The mechanism of thrombosis with this syndrome is complex and not well understood. However, it is plausible that anti-phospholipid antibodies predispose to premature atherosclerosis which increases the risk of infarction with his syndrome4.
    • Coronary artery spasm
      • Coronary artery spasm (CAS) is probably the predominant mechanism for myocardial infarction with the use of cocaine. Cocaine has been associated with angina, myocardial infarction, tachyarrhythmia’s and bradyarrhythmias, sudden cardiac death and myocardial contraction bands, which can possibly act as a substrate for arrhythmias. The cardiac effects of cocaine are mediated through four main pathways
        1. Endothelial dysfunction which predisposes to vasoconstriction and thrombosis.
        2. Promotion of atherosclerosis
        3. Increased myocardial oxygen demand due to an acute rise in systemic blood pressure and heart rate.
        4. Coronary vasoconstriction caused by its α1- adrenergic properties and calcium dependent direct vasoconstriction5.
    • Coronary embolization
      • Coronary artery embolism is a rare cause of acute myocardial infarction (AMI) and the precise diagnosis remains challenging for the interventional cardiologist. The true prevalence of this nonatherosclerotic entity remains vague because of its difficult diagnosis in the acute setting.
    • Myocardial bridging
      • This is a congenital anomaly in which the coronary artery is embedded within the subepicardial myocardium or has a band of myocardium overlying it. This can impede blood flow during systole that can persist during diastole resulting in myocardial ischemia3.

Angiographically abnormal coronary arteries

We know that even angiographically “normal” looking coronary arteries can still have significant atherosclerotic plaque, and not surprisingly, can still result in myocardial infarction. Therefore, the definition of normality is arbitrary and not definite.

  • Accelerated atherosclerosis
    • The true prevalence of advanced coronary atheroma in young adults is not well studies. An autopsy study of 760 victims of accidents, suicide and homicides aged 15-34 years found advanced coronary atheroma in 2% of males aged 15-19 years and none in women. This reveals that being male solemnly is a risk factor for atherosclerosis. Additionally, in the 30-34 age group, about 20% of men and 8% of women had advanced coronary atheroma. It is known that genetic mutation in the low density lipoprotein receptor produces familial hypercholesterolemia, an autosomal dominant disorder characterized by premature atherosclerosis and high serum cholesterol. Various other lipid fractions and hyperhomocysteinaemia are implicated in premature atherosclerosis and MI3.
  • Aneurysm and anomalous origin of arteries dissection
    • Coronary artery aneurysm are congenital or acquired secondary to Kawasaki’s disease in childhood. They have been linked to myocardial infarction in young adults, although the actual mechanism is not well understood.
  • Spontaneous dissection
    • Spontaneous dissection is a condition with great prevalence in women, especially in the peripartum or early postpartum period. However, it is a rare cause of MI6.

 

REFERENCES:

  1. Wong CP, Loh SY, Loh KK, Ong PJ, Foo D, Ho HH. Acute myocardial infarction: Clinical features and outcomes in young adults in Singapore. World J Cardiol. 2012;4(6):206–210. doi:10.4330/wjc.v4.i6.206
  2. Sinha SK, Krishna V, Thakur R, et al. Acute myocardial infarction in very young adults: A clinical presentation, risk factors, hospital outcome index, and their angiographic characteristics in North India-AMIYA Study. ARYA Atheroscler. 2017;13(2):79–87.
  3. Osula S, Bell GM, Hornung RS. Acute myocardial infarction in young adults: causes and management. Postgrad Med J. 2002;78(915):27–30. doi:10.1136/pmj.78.915.27
  4. Turrent-Carriles A, Herrera-Félix JP, Amigo MC. Renal Involvement in Antiphospholipid Syndrome. Front Immunol. 2018;9:1008. Published 2018 May 17. doi:10.3389/fimmu.2018.01008
  5. Hung MJ, Hu P, Hung MY. Coronary artery spasm: review and update. Int J Med Sci. 2014;11(11):1161–1171. Published 2014 Aug 28. doi:10.7150/ijms.9623
  6. Adlam D, Alfonso F, Maas A, Vrints C; Writing Committee. European Society of Cardiology, acute cardiovascular care association, SCAD study group: a position paper on spontaneous coronary artery dissection. Eur Heart J. 2018;39(36):3353–3368. doi:10.1093/eurheartj/ehy080

 

The views, opinions and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your personal health matters. If you think you are having a heart attack, stroke or another emergency, please call 911 immediately.

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Late Breaking Science DAPA-HF: SGLT-2 inhibitors might influence Cardiovascular outcomes—- Benefits extend above and beyond HbA1c.

The DAPA-HF trial was definitely the highlight of the scientific sessions at the AHA19 conference. I’m fascinated by the interesting outcomes and keen to learn more about the effect of SGLT-2 inhibitors on heart failure (HF) patients with preserved ejection fraction (HFpEF). In the next few lines, I’m going to briefly discuss the significant findings of DAPA-HF that were presented at AHA19, and will sooner nor later change the guidelines for management of patients with HFrEF.

Sodium-glucose cotransporter-2 inhibitor (SGLT-2 inhibitor) are relatively new class of drugs that act on inhibiting glucose reabsorption from proximal tubules, and thus decrease serum blood glucose concentrations.1 They are commonly prescribed to treat T2DM patients who have poor glycemic control. However, new data are emerging in large support of the beneficial effects of SGLT-2 inhibitors not just on diabetics but also on non-diabetic HF patients. The data is big and clear as presented by Dr. John McMurray at AHA19 and it is expected to list SGLT-2 inhibitors such as dapagliflozin (Farxiga) as guideline directed medical therapeutics (GDMT) in 2021 for HF patients.

In the DAPA-HF, McMurray and colleagues enrolled 4,744 patients with heart failure characterized by reduced ejection fraction (defined as left ventricle ejection fraction of 40% or less) from 20 different countries. There were 2,139 patients diagnosed with diabetes who were more likely to have HF etiology of ischemia when compared to non-diabetic patients with HF. The study population consisted of high risk middle aged patients with a mean LV ejection fraction of 31%. The primary end point was a composite outcome consisted of cardiovascular death, HF hospitalization and urgent HF hospital visits over an average of 18 months. As for diabetics in the DAPA-HF trial there was a 25% reduction of CV events (HR 0.75, 95% CI 0.63-0.90) when comparing dapagliflozin against placebo. While, there was a 27% reduction among those who did not have diabetes (HR 0.73, 95% CI 0.59-0.91).2

“The relative and absolute risk reduction in death and hospitalization were substantial, clinically important and consistent across the age spectrum and baseline health status in both patients with or without diabetes”, McMurray noted.

The mechanism by which dapagliflozin provides the cardiovascular benefits that has been documented in the DAPA- HF trial remains to be unclear. It is plausible that SGLT-2 inhibition modifies many CV risk factors such as BP, visceral adiposity, arterial stiffness, hyperinsulinemia, albuminuria, circulating uric acid levels and oxidative stress. These factors are involved in several pathways related to the cardiorenal outcome, where SGLT-2 inhibitors regulate the glucose and sodium excretion and therefore modify the factors in these pathways.

Below is an illustration that explains the proposed pathways involved in cardioprotective role of SGLT-2 inhibitors3

dapahf

In conclusion, dapagliflozin offers new approaches to the treatment of HF with reduced ejection fraction (HFrEF) in patients with or without diabetes. Data from the DAPA-HF trail provides robust support for the initiation of SGLT-2 inhibitors in patients who either have an established CVD or at risk of developing CVD, and HF in particular, or at risk for renal decline and progression into chronic kidney disease (CKD).

 

References:

  1. Mcmurray, John J. V., Demets, David L., Inzucchi, Silvio E., et al. A trial to evaluate the effect of the sodium–glucose co‐transporter 2 inhibitor dapagliflozin on morbidity and mortality in patients with heart failure and reduced left ventricular ejection fraction (DAPA‐HF. European Journal of Heart Failure. 2019;21(5):665-675. doi:10.1002/ejhf.1432
  2. Packer, Milton. Lessons learned from the DAPA-HF trial concerning the mechanisms of benefit of SGLT2 inhibitors on heart failure events in the context of other large-scale trials nearing completion. Cardiovascular diabetology. 2019;18(1):129. doi:10.1186/s12933-019-0938-6
  3. Ali, Amar, Bain, Steve, Hicks, Debbie, et al. SGLT2 Inhibitors: Cardiovascular Benefits Beyond HbA1c-Translating Evidence into Practice. Diabetes therapy : research, treatment and education of diabetes and related disorders. 2019;10(5):1595-1622. doi:10.1007/s13300-019-0657-8

 

The views, opinions and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your personal health matters. If you think you are having a heart attack, stroke or another emergency, please call 911 immediately.