Sick Sinus Syndrome

Sick Sinus Syndrome

Sick Sinus Syndrome | Johns Hopkins Medicine

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Sick sinus syndrome (SSS) is a disease in which the heart's natural pacemaker located in the upper right heart chamber (right atrium) becomes damaged and is no longer able to generate normal heartbeats at the normal rate. It may be a result of other medical conditions that damage the sinoatrial node (SA node) over time or may be a result of certain medicines. This can result in heartbeats that are too slow, too fast ⁠— or heartbeats that alternate between slow and fast. 

What causes sick sinus syndrome?

Any condition that can cause heart damage can damage the SA node.

This includes:

  • Coronary artery disease
  • Prior heart attack
  • Atrial fibrillation
  • Heart failure or cardiomyopathy
  • Taking certain medicines such as beta blockers, calcium channel blockers, digoxin, and antiarrhythmics
  • Severe hypothyroidism
  • Inflammatory conditions that involve the heart (rheumatic fever, Chagas disease, pericarditis, myocarditis)
  • Infiltrative heart diseases (sarcoidosis, amyloidosis, scleroderma, hemochromatosis)
  • Electrolyte abnormalities such as high potassium levels
  • Rare familial disease
  • Trauma

Hypothyroidism, hypothermia, and electrolyte problems are generally reversible.

What are the risk factors for sick sinus syndrome?

Sick sinus syndrome affects men and women equally, and can occur at any age. But most cases of SSS occur in people over age 70, because aging tends to slow the heart rate and lower SA node function.

You are at greater risk for SSS if you have any of the following conditions:

  • Coronary artery disease or history of heart attack
  • Heart failure or cardiomyopathy
  • Atrial fibrillation
  • Inflammatory conditions that can involve the heart such as rheumatic fever, pericarditis, Chagas disease, or myocarditis
  • Infiltrative heart diseases such as sarcoidosis, amyloidosis, hemochromatosis, or scleroderma
  • Hypothyroidism
  • Rare familial diseases
  • Trauma

You are also at greater risk of you take medicines such as beta blockers, calcium channel blockers, digoxin, antiarrhythmics.

What are the symptoms of sick sinus syndrome?

You may have sick sinus syndrome with few or no symptoms. If you do have symptoms, they may include:

  • Dizziness
  • Fainting
  • Shortness of breath, especially with exertion
  • Heart palpitations
  • Chest pain

How is sick sinus syndrome diagnosed?

Your healthcare provider may suspect sick sinus syndrome your symptoms, but they are common in many other diseases. To diagnose your condition, your healthcare provider will do an electrocardiogram (ECG). This is a machine that records your heart's rate and rhythm. If you do not have symptoms at the time of your ECG, it may look normal.

Other possible tests include:

  • An ECG while you walk on a treadmill (stress test)
  • A Holter monitor, a recorder you wear for over 24 hours that takes an ECG
  • An event recorder, a recorder you wear over several days that samples your heart rate
  • Electrophysiologic testing, a hospital procedure that involves threading catheters into your heart through a vein in your thigh
  • Echocardiogram or ultrasound of your heart, which checks for structural heart problems

How is sick sinus syndrome treated?

You may have sick sinus syndrome without symptoms and not need treatment. However, if you do have symptoms and need treatment, there are options, such as:

  • Medicine change. Your healthcare provider may change your medicines if you are taking any known to cause sick sinus syndrome.
  • Blood thinners. Because there is an increased risk for blood clots forming in your heart and causing a stroke, you may need to take a blood thinner as a preventive step.
  • Pacemaker. The most common treatment for people with symptoms that do not have an identifiable reversible causes is a pacemaker implant. This is a small, battery-powered device that takes the place of your SA node and regulates your heart rate. A doctor places a pacemaker under the skin of your chest during a minor surgical procedure. Wires are placed within the heart that can monitor the heart rate and stimulate the heartbeat when needed.

What are the complications of sick sinus syndrome?

Sick sinus syndrome often progresses over time. When your heart beats too slowly, or too quickly,  it can lead to complications:

  • You may be injured if you pass out during an arrhythmia.
  • Cardiac blood flow may be impaired leading to other organ damage such as brain and kidney function

Living with sick sinus syndrome

The aging of your SA node causes most cases of sick sinus syndrome, and there’s no way to prevent that. But you can help prevent complications by learning as much as you can about the disease and working closely with your cardiologist to find the best treatment.

You can also make healthy lifestyle changes:

  • Don't smoke.
  • Work with your healthcare provider to keep conditions high cholesterol and high blood pressure under control.
  • Eat a heart-healthy diet.
  • Maintain a healthy weight.
  • Get regular exercise.
  • Tell your healthcare provider if you have any symptoms.

Key points

  • Sick sinus syndrome is a slow heart rate.
  • The most common cause is a gradual loss of SA node function that comes with age.
  • You may have no symptoms or you may experience dizziness, fainting, shortness of breath, or fatigue.
  • Sick sinus syndrome may be treated by changing your medicines, treating underlying medical conditions, or inserting a pacemaker.
  • Not smoking, keeping your cholesterol and blood pressure under control, eating a healthy diet, maintaining a healthy weight, and getting regular exercise can help reduce the risk of sick sinus syndrome.

Next steps

Tips to help you get the most from a visit to your healthcare provider:

  • Know the reason for your visit and what you want to happen.
  • Before your visit, write down questions you want answered.
  • Bring someone with you to help you ask questions and remember what your provider tells you.
  • At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you.
  • Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side effects are.
  • Ask if your condition can be treated in other ways.
  • Know why a test or procedure is recommended and what the results could mean.
  • Know what to expect if you do not take the medicine or have the test or procedure.
  • If you have a follow-up appointment, write down the date, time, and purpose for that visit.
  • Know how you can contact your provider if you have questions.

Source: https://www.hopkinsmedicine.org/health/conditions-and-diseases/sick-sinus-syndrome

Bioartificial Sinus Node Constructed via In Vivo Gene Transfer of an Engineered Pacemaker HCN Channel Reduces the Dependence on Electronic Pacemaker in a Sick-Sinus Syndrome Model

Sick Sinus Syndrome | Johns Hopkins Medicine

Background— The normal cardiac rhythm originates in the sinoatrial (SA) node that anatomically resides in the right atrium.

Malfunction of the SA node leads to various forms of arrhythmias that necessitate the implantation of electronic pacemakers.

We hypothesized that overexpression of an engineered HCN construct via somatic gene transfer offers a flexible approach for fine-tuning cardiac pacing in vivo.

Methods and Results— Using various electrophysiological and mapping techniques, we examined the effects of in situ focal expression of HCN1-ΔΔΔ, the S3-S4 linker of which has been shortened to favor channel opening, on impulse generation and conduction.

Single left ventricular cardiomyocytes isolated from guinea pig hearts preinjected with the recombinant adenovirus Ad-CMV-GFP-IRES-HCN1-ΔΔΔ in vivo uniquely exhibited automaticity with a normal firing rate (237±12 bpm).

High-resolution ex vivo optical mapping of Ad-CGI-HCN1-ΔΔΔ–injected Langendorff-perfused hearts revealed the generation of spontaneous action potentials from the transduced region in the left ventricle.

To evaluate the efficacy of our approach for reliable atrial pacing, we generated a porcine model of sick-sinus syndrome by guided radiofrequency ablation of the native SA node, followed by implantation of a dual-chamber electronic pacemaker to prevent bradycardia-induced hemodynamic collapse.

Interestingly, focal transduction of Ad-CGI-HCN1-ΔΔΔ in the left atrium of animals with sick-sinus syndrome reproducibly induced a stable, catecholamine-responsive in vivo “bioartificial node” that exhibited a physiological heart rate and was capable of reliably pacing the myocardium, substantially reducing electronic pacing.

Conclusions— The results of the present study provide important functional and mechanistic insights into cardiac automaticity and have further refined an HCN gene–based therapy for correcting defects in cardiac impulse generation.

The normal cardiac rhythm originates in the sinoatrial (SA) node that anatomically resides in the right atrium (RA). Malfunctions of the SA node due to aging or disease lead to various forms of arrhythmias that necessitate the implantation of electronic pacemakers.

If, encoded by the hyperpolarization-activated cyclic-nucleotide–modulated (HCN) channel gene family,1 is a key player in pacing, although its mechanistic role remains to be fully dissected. Pathophysiologically, human HCN mutations have been linked to sinus node dysfunction.

2,3 To date, 4 isoforms, namely, HCN1, HCN2, HCN3, and HCN4, each with a distinct pattern of tissue distribution and biophysical profiles, have been identified.

4–9 Of the 2 predominant isoforms in the SA node, time-dependent HCN1 currents open &40 times faster than those of HCN4 channels10–14; the fastest isoform, HCN1, activates at approximately −80 mV, with opening time constants in the range of seconds.

HCN1, HCN2, HCN3, and HCN4 readily coassemble (except between HCN2 and HCN3) in different stoichiometries to form heterotetramers with properties that cannot be readily predicted from the individual isoforms.10,15,16 Therefore, native If has a complex molecular identity that depends on the species, tissue type, and particular isoforms expressed.

Furthermore, HCN channels activate at more positive voltages in neonatal cardiomyocytes (CMs) than in their adult counterparts and other mammalian expression systems, which suggests that the gating properties of If are also highly context-dependent.

17 Although overexpression of HCN1 or HCN2 in spontaneously firing, If-expressing neonatal left ventricular (LV) cells hastens their firing rate,18,19 neither of the wild-type (WT) channels alone suffices to induce pacing in quiescent adult LV CMs that intrinsically lack If presumably due to their negative activation profiles.

20 Thus, native If is difficult to reproduce by simple expression of a single HCN isoform.

Here, we took advantage of the engineered construct HCN1-EVY235-7ΔΔΔ(or HCN1-ΔΔΔ) channels, the S3-S4 linker of which has been systematically shortened by deleting residues 235 to 237 to favor channel opening21,22 and thereby compensate for any context-dependent gating effects.

We conjectured that overexpressing EVY235-7ΔΔΔ channels alone in atrial or ventricular CMs can sufficiently mimic the heteromultimeric native nodal If without the need for simultaneous manipulation of the expression levels of multiple HCN isoforms and/or other modifying subunits and factors that may be present in nodal but not muscle cells.

Indeed, our experiments show that HCN1-ΔΔΔ channels, when expressed in native ventricular or atrial CMs, exhibit biophysical properties that better mimic those of the heteromultimeric native nodal If than WT channels. To further explore the potential of engineered HCN channels for therapies, the effects of in situ focal expression of HCN1-ΔΔΔ in the left atrium (LA) or LV on impulse generation and conduction were examined with various ex vivo and in vivo mapping techniques.

Adenovirus-Mediated Gene Transfer

Polymerase chain reaction–based mutagenesis of mouse HCN1 (generously provided by Dr Steve Siegelbaum, Columbia University, New York, NY) of the bicistronic adenovirus shuttle vector pAdCMV-GFP-IRES (or pAdCGI) was performed with overlapping oligonucleotides as described in our previous publications.

22,23 The internal ribosomal entry site allows the simultaneous translation of 2 transgenes with a single transcript, and in the present experiments, green fluorescent protein (GFP) and an HCN1 construct.

HCN1-ΔΔΔ was cloned into the second position of pAdCGI at EcoRI and XmaI to generate pAdCGI-HCN1-ΔΔΔ. Adenoviruses were generated by Cre-lox recombination of purified ψ5 viral DNA and shuttle vector DNA with Cre4 cells.

The recombinant products were plaque purified, amplified, and purified again by CsCl gradients, which yielded concentrations of the order of 1010 plaque-forming units (PFU) mL−1.

Intracardiac Injection and Isolation of LV CMs

Adenoviruses (150 μL) with a concentration on the order of 1010 PFU/mL were injected subepicardially with a 21-gauge needle into the LV anterior wall (&1 mm deep) of anesthetized adult breeder guinea pigs (weight &250 g; Charles River Laboratories, Wilmington, Mass) after thoracotomy and during transient cross-clamping of the great vessels.

The area of injection (anterior epicardium, midway between the apex and base) was chosen because it is most suitable for mapping owing to minimal heart curvature; thus, motion artifacts can be suppressed by gentle stabilization.

A small suture in the immediate vicinity of the injected area was typically introduced at the time of injection to further assist our identification of the region of interest during the mapping experiments. Furthermore, a parallel optical port was designed to enable visualization of the exact mapped area, which was aligned to include the injected region and its surroundings.

Injected animals were allowed to recover from the surgical procedure for 72 to 96 hours. For isolation of CMs, animals were euthanized by intraperitoneal injection of pentobarbital (80 mg/kg).

The hearts were quickly excised, followed by perfusion with enzymatic solutions using a customized Langendorff apparatus (Harvard Apparatus, Holliston, Mass) as described previously,24 and recorded within 24 hours. As needed, porcine atrial CMs were similarly isolated. A typical image of positively transduced LV CMs freshly isolated from an injected heart is provided in Figure I of the online Data Supplement.

High-Resolution Ex Vivo Optical Mapping

To determine whether focal transduction could capture the myocardium, we used the same animal model and optical mapping system that we recently reported.

24 In brief, after surgical dissection of the RA, a specialized cryoprobe was inserted into the right ventricular (RV) cavity and placed in contact with the high septum, 1 mm below the base of the heart; liquid nitrogen was then rapidly and continuously passed through the probe via a commercially available cryogun (Brymill Inc, Ellington, Conn) for 2 minutes, which resulted in ablation of the RV-facing septum and the endocardial surface of the basal RV free wall but not the LV. This procedure resulted in a marked suppression of the intrinsic guinea pig heart rate (

Source: https://www.ahajournals.org/doi/10.1161/circulationaha.106.615385

Johns Hopkins Vasculitis Center

Sick Sinus Syndrome | Johns Hopkins Medicine

The symptoms of vasculitis depend on the particular blood vessels that are involved by the inflammatory process.

Different types of vasculitis involve blood vessels in characteristic locations throughout the body.

For example, Giant Cell Arteritis typically involves the medium– to large–sized blood vessels supplying the head and neck, but rarely involves the blood vessels of the kidneys.

In contrast, Wegener’s Granulomatosis (GPA) frequently involves the kidneys, very often the lungs, and almost always the upper respiratory tract, but rarely blood vessels to the brain.

As depicted in the image, Buerger’s disease involves the fingers and (toes). Gangrene can result from a profound lack of blood flow.

Different types of vasculitis have characteristic (localized) patterns of blood vessel involvement.  However, vasculitis is a systemic illness. Thus, patients with vasculitis feel sick.

They often have fevers, weight loss, fatigue, a rapid pulse, and diffuse aches and pains that are difficult to pinpoint.

It has been said that vasculitis is a “hurting disease”, because it is so commonly associated with pain of one type or another: pain from a nerve infarction, pain from insufficient blood to the gastrointestinal tract, pain from skin ulcers.

In some cases, however, identifying the source and underlying cause of the pain is extremely challenging.  In addition to these diffuse, poorly–localized “constitutional symptoms”, vasculitis may involve virtually every organ system in the body.

What organ systems may be affected?

It is important to note that not every organ system will be affected in every patient. The pattern of organ involvement (and symptoms) is unique to the individual, as well as the type of vasculitis (category).

Skin

A variety of rashes, the most classic of which is “palpable purpura” –purplish–red spots, usually found on the legs. These spots can usually be felt by the examiner’s fingertips, hence the descriptor “palpable”.

This is a classic example of palpable purpura. These lesions result from the leakage of blood into the skin through inflamed, damaged blood vessels. They tend to occur in “crops”.

Repeated bouts of purpura may lead to hyperpigmented areas of the skin.

Joints

Symptoms range from full–blown arthritis to aches in the joints without obvious swelling (arthralgias).

This is an example of Henoch-Schönlein purpura: cutaneous vasculitis manifested by palpable purpura and arthritis (note the right ankle swelling). The diagnosis was confirmed by a skin biopsy, with immunofluorescence positive for IgA deposition witin blood vessel walls.

Lungs

Cough (particularly coughing up blood), shortness of breath, a pneumonia– appearance to a patient’s chest X–ray, lung “infiltrates”, and the development of cavities in the lungs.

In this image of a CAT scan of the lungs of a 73 year–old woman complaining of constitutional symptoms, shortness of breath, and bloody sputum. The patient also had glomerulonephritis, a positive P–ANCA, and antibodies to myeloperoxidase. The diagnosis of microscopic polyangiitis was made.

Eleven days later, as the patient’s symptoms worsened, a chest X–ray confirmed progression of her lung hemorrhage. The X–ray shows fluffy infiltrates in both lungs, representing bleeding from damaged capillaries.

Kidneys

Red blood cells (usually invisible to the naked eye), clumps of red blood cells (known as “casts”, also invisible to the naked eye), and loss of protein in the urine. May lead to renal insufficiency and the requirement of dialysis.

Depicted in the figure right is a single glomerulus (the filtering unit of the kidneys; each kidney has approximately 1 million glomeruli). This glomerulus is involved actively by an inflammatory process, particularly evident in the bottom of the figure.

Abdominal pain, bloody diarrhea, perforation of the intestines.

Anemia (low hematocrit or red blood cell count) and/or a slightly elevated white blood cell count.

Sinus, Nose & Ears

Chronic sinus congestion and “infections” that persist for longer than they should; hearing loss; inflammation of the nasal septum, sometimes resulting in a perforation or collapse of the bridge of the nose, as shown in the picture below.

Eyes

May affect either blood vessels to the eyes, causing the sudden loss of vision, or small blood vessels withinthe eyes, leading to retinal problems, thinning of the sclera (the white part of the eyes), inflammation within the eye’s different chambers, and conjunctivitis (“pinkeye”). Pictured below is an example of retinal vasculitis in a patient with systemic lupus erythematosus (lupus). The white areas represent regions of retinal infarction caused by vasculitis.

Brain

Headaches, strokes, changes in mental status, difficulty with coordination. Below, a magnetic resonance (MR) imaging study of the brain in central nervous system vasculitis demonstrates an intra–cerebral hemorrhage (bright area).

Nerve

Shooting pains in the arms and legs, numbness, and asymmetrical weakness (i.e., weakness that involves one side of the body more than the other).

All information contained within the Johns Hopkins Vasculitis Center website is intended for educational purposes only. Visitors are encouraged to consult other sources and confirm the information contained within this site. Consumers should never disregard medical advice or delay in seeking it because of something they may have read on this website.

Source: https://www.hopkinsvasculitis.org/vasculitis/symptoms-vasculitis/

Online Mendelian Inheritance in Man (OMIM)

Sick Sinus Syndrome | Johns Hopkins Medicine

  1. Bacos, J. M., Eagan, J. T., Orgain, E. S. Congenital familial nodal rhythm. Circulation 22: 887-895, 1960. [PubMed: 13685714] [Full Text: http://www.ahajournals.org/doi/full/10.1161/01.cir.22.5.887?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed]

  2. Bertram, H., Paul, T., Beyer, F., Kallfelz, H. C. Familial idiopathic atrial fibrillation with bradyarrhythmia. Europ. J. Pediat. 155: 7-10, 1996. [PubMed: 8750801] [Full Text: https://dx.doi.org/10.1007/bf02115617]

  3. Beyer, F., Paul, T., Luhmer, I., Bertram, H., Kallfelz, H. C. Familiaeres idiopathisches Vorhofflimmern mit bradyarrhythmie. Z. Kardiol. 82: 674-677, 1993. [PubMed: 8291288]

  4. Caralis, D. G., Varghese, P. J. Familial sinoatrial node dysfunction: increased vagal tone a possible aetiology. Brit. Heart J. 38: 951-956, 1976. [PubMed: 971377] [Full Text: http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=971377]

  5. Lehmann, H., Klein, U. E. Familial sinus node dysfunction with autosomal dominant inheritance. Brit. Heart J. 40: 1314-1316, 1978. [PubMed: 718774] [Full Text: http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=718774]

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  7. Milanesi, R., Baruscotti, M., Gnecchi-Ruscone, T., DiFrancesco, D. Familial sinus bradycardia associated with a mutation in the cardiac pacemaker channel. New Eng. J. Med. 354: 151-157, 2006.

    Note: Erratum: New Eng. J. Med. 354: 2520 only, 2006. [PubMed: 16407510] [Full Text: http://www.nejm.org/doi/full/10.1056/NEJMoa052475?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.

    org&rfr_dat=cr_pub%3dpubmed]

  8. Milano, A., Vermeer, A. M. C., Lodder, E. M., Barc, J., Verkerk, A. O., Postma, A. V., van der Bilt, I. A. C., Baars, M. J. H., van Haelst, P. L., Caliskan, K., Hoedemaekers, Y. M., Le Scouarnec, S., Redon, R., Pinto, Y. M., Christiaans, I., Wilde, A. A.

    , Bezzina, C. R. HCN4 mutations in multiple families with bradycardia and left ventricular noncompaction cardiomyopathy. J. Am. Coll. Cardiol. 64: 745-756, 2014. [PubMed: 25145517] [Full Text: https://linkinghub.elsevier.

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  9. Nof, E., Luria, D., Brass, D., Marek, D., Lahat, H., Reznik-Wolf, H., Pras, E., Dascal, N., Eldar, M., Glikson, M.

    Point mutation in the HCN4 cardiac ion channel pore affecting synthesis, trafficking, and functional expression is associated with familial asymptomatic sinus bradycardia. Circulation 116: 463-470, 2007.

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  10. Schulze-Bahr, E., Neu, A., Friederich, P., Kaupp, U. B., Breithardt, G., Pongs, O., Isbrandt, D. Pacemaker channel dysfunction in a patient with sinus node disease. J. Clin. Invest. 111: 1537-1545, 2003. [PubMed: 12750403] [Full Text: https://doi.org/10.1172/JCI16387]

  11. Schweizer, P. A., Duhme, N., Thomas, D., Becker, R., Zehelein, J., Draguhn, A., Bruehl, C., Katus, H. A., Koenen, M.

    cAMP sensitivity of HCN pacemaker channels determines basal heart rate but is not critical for autonomic rate control. Circ. Arrhythm. Electrophysiol. 3: 542-552, 2010. [PubMed: 20693575] [Full Text: http://www.

    ahajournals.org/doi/full/10.1161/CIRCEP.110.949768?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed]

  12. Schweizer, P. A., Schroter, J., Greiner, S., Haas, J., Yampolsky, P., Mereles, D., Buss, S. J., Seyler, C., Bruehl, C., Draguhn, A., Koenen, M., Meder, B., Katus, H. A., Thomas, D.

    The symptom complex of familial sinus node dysfunction and myocardial noncompaction is associated with mutations in the HCN4 channel. J. Am. Coll. Cardiol. 64: 757-767, 2014.

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  13. Surawicz, B., Hariman, R. J. Follow-up of the family with congenital absence of sinus rhythm. Am. J. Cardiol. 61: 467-469, 1988. [PubMed: 3341232] [Full Text: https://linkinghub.elsevier.com/retrieve/pii/0002-9149(88)90309-8]

  14. Ueda, K., Nakamura, K., Hayashi, T., Inagaki, N., Takahashi, M., Arimura, T., Morita, H., Higashiuesato, Y., Hirano, Y., Yasunami, M., Takishita, S., Yamashina, A., Ohe, T., Sunamori, M., Hiraoka, M., Kimura, A.

    Functional characterization of a trafficking-defective HCN4 mutation, D553N, associated with cardiac arrhythmia. J. Biol. Chem. 279: 27194-27198, 2004. [PubMed: 15123648] [Full Text: http://www.jbc.

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  15. Vermeer, A. M. C., Lodder, E. M., Thomas, D., Duijkers, F. A. M., Marcelis, C., van Gorselen, E. O. F., Fortner, P., Buss, S. J., Mereles, D., Katus, H. A., Wilde, A. A. M., Bezzina, C. R., Boekholdt, S. M., Matthijs Boekholdt, S., Schweizer, P. A.

    , Christiaans, I. Dilation of the aorta ascendens forms part of the clinical spectrum of HCN4 mutations. (Letter) J. Am. Coll. Cardiol. 67: 2313-2315, 2016. [PubMed: 27173043] [Full Text: https://linkinghub.elsevier.

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Source: https://www.omim.org/entry/163800

JHU HR Information Regarding Novel Coronavirus – JHU Human Resources

Sick Sinus Syndrome | Johns Hopkins Medicine

What is happening with the JHU contribution to retirement plans?
Because of the COVID-19 pandemic, the university faces the prospect of large operating losses this fiscal year and next.

Among the first set of steps the university has taken to address those potential projected shortfalls is a one-year suspension of university contributions to most retirement plans from July 1, 2020 through June 30, 2021.

Learn more about the details here.

What does my JHU health insurance cover?
The JHU health plan has waived copays and deductibles associated with testing for COVID-19. If you have additional benefits questions, contact the Benefits Service Center at 410-516-2000 or benefits@jhu.edu.

How are telehealth visits being covered?
All JHU medical plans will cover any telehealth visit at 100% with no cost to the patient.

Your healthcare provider may submit claims under the telehealth code, and they will be covered for dates of service starting on February 4, 2020 and continuing for the duration of the public health crisis.

You also have access to a telehealth app through the insurance provider. This allows you to receive care when you need it or if your routine provider is not available.

How do I access the telehealth apps?
Each health plan has access to a telehealth app that allows you to get the care you need, when and where you need it. You can talk with a doctor by video on your smartphone, tablet, or computer.

You can see a provider online if you need treatment for a common condition such as a sinus infection or a sore throat.

For mental health, diet/nutrition, or breastfeeding support, you can schedule a virtual visit and meet with a licensed professional from the comfort of your home.

  • CareFirst Members: Download the CareFirst Video Visit app and enter your insurance information from your CareFirst card.
  • EHP Members: EHP member may also use the CareFirst Video Visit by entering the coupon code: JHU-COVID19. The code is valid for all video visit services until June 30, 2020. When you reach the insurance information section during registration, select “other/my insurance is not listed.” Following that step, you will have the opportunity to enter the coupon code.
  • Kaiser Members:  You must register with KP.org to get started using telehealth services.

What options do I have to refill my prescriptions?
We highly encourage switching to mail order for all maintenance medications. This program allows a full 90 days to be mailed directly to your home address with no need to leave the house. Click here for instructions on how to set up your mail order.

If you are covered by JHU health insurance, Express Scripts offers 1 additional emergency refill. This allows you to refill your prescription immediately after picking up a prior refill, and no special approval is necessary. You should advise your pharmacy that you are requesting an “Emergency Refill.”

Due to concerns around retail supply, this should only be used for emergencies and some pharmacies may be limiting quantities. Click here to visit Express Scripts’ COVID resource page.

I am currently enrolled in the Dependent Care Flexible Spending Account, but my childcare (or my child’s camp) has closed or has changed. Can I stop my deductions?
Yes, if you no longer are paying for care you may stop you current DCFSA deductions. Deductions may only be stopped prospectively, and you cannot revoke your full election.

To make a change to your election, log into the Benefits Enrollment Portal by clicking on myChoices Health and Life Enrollment from the main page of the Benefits site. From there, click on Start a Qualified Life Event – Family Changes. When your childcare needs return, you can restart the deductions through the portal.

For additional assistance or questions please reach out to the Benefits Service Center or call 410-516-2000 for assistance.

How do I cancel my pre-tax commuter benefits?
Commuter benefits can be canceled and restarted at any time throughout the year. To make changes to your commuter elections, log into the Benefits Enrollment Portal by clicking on myChoices Health and Life Enrollment from the main page of the Benefits site. From there, click on Start a Qualified Life Event – Commuter Changes.

Are EyeMed benefits available to members online?
Yes. EyeMed members have multiple options to order prescription eyewear and contact lenses online using their benefits. This may be an ideal solution to practice social distancing and mitigate outdoor risk. Online sites will require a valid prescription.

Online, in-network options include: Glasses.com, ContactsDirect, Ray-Ban.com, LensCrafters.com, and TargetOptical.com. Under the current circumstances, many of these online providers are offering free, expedited shipping and no-cost returns for extra convenience. Members should check with the online providers to verify offers.

An EyeMed Member FAQ is also available. Questions can be directed to EyeMed’s Customer Care Center for JHU at 866-800-5457 or their general Customer Care Center at 1-866-933-3633.

I need to withdraw money from my 403(b) retirement account to cover expenses related to the COVID-19 pandemic.  Am I eligible?
Under the Coronavirus Aid, Relief, and Economic Security Act (CARES Act) an employee may qualify and be eligible for a coronavirus-related distribution, if they meet one of the criteria below and self-certify through their investment provider.

  • You, your spouse, or dependent was diagnosed with coronavirus;
  • You have experienced adverse financial consequences as a result of being quarantined, furloughed or laid off, or your work hours have been reduced;
  • You are unable to work because of a lack of child care;
  • You have had to close or reduce the hours of a business as a result of the virus; or
  • You have been financially impacted by other factors determined by the US Secretary of Treasury.

Is there a cap on how much I can withdraw?
Yes.  During 2020, you may withdraw up to a total of $100,000 in coronavirus-related distributions from your employee contributions or any rollover funds in the JHU 403(b) plan.  The university’s 457(b) plan is not eligible under the coronavirus-related withdrawal rules.

Will I have to pay an early withdrawal penalty if I take a coronavirus-related distribution?
No.  Under the CARES Act, the 10-percent tax penalty that generally applies to early withdrawals from a retirement account if you are younger that 591/2  is waived for coronavirus-related withdrawals taken between January 1 and December 31, 2020.

Do I have to pay a tax on these distributions?
Yes.  However, the tax associated with the distributions may be paid ratably over three years, beginning with taxable year 2020.

  The CARES Act also allows you to recontribute the funds you withdrew back to your retirement account without interest in one or more payments within three years.

The recontributed amounts will not count toward the annual contribution limit in the year that the funds are returned to your 403(b).

Are there any changes regarding loans from retirement plans?
Yes.

  The amount you can borrow from your 403(b) plan increased from $50,000 to $100,000 or 100% (at Fidelity only) of your employee contributions and any rollover funds, whichever is less.

  The increased loan limit is only available from March 27, 2020 through September 22, 2020.  Loans may be obtained through your retirement accounts with Fidelity and TIAA, if applicable.

If you already have an outstanding loan, all loan payments due between March 27, 2020 through December 31, 2020 can be deferred for up to one year, but interest will continue to accrue and the loan will be re-amortized when the loan repayments restart in 2021.  This means your loan repayment amount will increase when repayments start again.

How do I initiate a coronavirus distribution or loan payment suspension?  
A CARES Act distribution or loan payment suspension is initiated by contacting your 403(b) investment provider directly.

  Completed forms (including notarized spousal signature) are to be emailed to the Benefits Service Center at benefits@jhu.edu for plan sponsor signature.

  The Benefits Service Center will forward the approved request to the investment provider for processing.

Source: https://hr.jhu.edu/coronavirus/