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  1. Sara Haddadi MD, Miami FL
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[1]

<nowiki>
 
 
 
 
 
 
 
 
Acute Cough
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
History and physical

examination, ask about environmental and occupational factors and travel exposures

± investigations
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Life-threatening diagnosis
 
 
 
 
 
 
 
 
 
 
 
Non-life-threatening diagnosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pneumonia, severe

exacerbation of asthma or COPD, PE, heart failure, other serious

disease
 
 
 
 
 
Infections
 
 
 
 
 
 
 
 
 
Exacerbation of pre-existing condition
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
LRTI
 
 
URTI
 
 
 
Asthma
 
Bronchiectasis
 
UACS
 
COPD
 
Evaluate and treat first
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Acute Bronchitis
 
 
 
Pertussis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Consider TB in

endemic areas

or high risk
 
 
 
 
 
 
 
 
 
 
 
 



<nowiki>
 
 
 
 
 
 
 
 
Acute Cough
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
History and physical

examination, ask about environmental and occupational factors and travel exposures

± investigations
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
C01
 
 
 
 
 
 
 
 
 
 
 
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D01'
D01
 
 
 
 
 
X
 
 
 
 
 
 
 
 
 
D02'
D02
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
LRTI
 
 
URTI
 
 
 
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E04
 
E01
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Y
 
 
 
Z
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
ZZ
 
 
 
 
 
 
 
 
 
 
 
 


Natural History, Complications and Prognosis

In a case series with 187 patients who had confirmed COVID-19, 27.8% of patients had a myocardial injury, which caused cardiac dysfunction and arrhythmias. The result was significantly higher mortality among patients with myocardial injury.

  • Based on the Troponin level The mortality during hospitalization was shown to be as below:
    • 7.62% for patients without underlying CVD and normal TnT levels
    • 13.33% for those with underlying CVD and normal TnT levels
    • 37.50% for those without underlying CVD but elevated TnT levels
    • 69.44% for those with underlying CVD and elevated TnTs.[2]


Classification of Infra-Hisian Block
Types of Infra-Hisian Block Sub-type
Type 2 second degree heart block (Mobitz II) _
Left bundle branch block Left anterior fascicular block
Right bundle branch block _


Covid19. [1]


underlying medical conditions that increase a person’s risk of severe illness from COVID-19
Level of Evidence Condition
Strongest and Most Consistent Evidence
  • Serious heart conditions, such as heart failure, coronary artery disease, or cardiomyopathies
  • Cancer
  • Chronic kidney disease
  • COPD
  • Obesity (BMI> 30)
  • Sickle cell disease
  • Solid organ transplantation
Mixed Evidence Left anterior fascicular block
Limited Evidence _
  1. Strongest and most consistent evidence: define as consistent evidence from multiple small studies or a strong association from a large study are categorized. They increase the severity of COVID-19 regardless of the individual's age:[3]
  2. Mixed evidence: Defined as multiple studies that reached different conclusions about the risk associated with a condition
  3. Limited evidence: Defined as consistent evidence from a small number of studies. Limited evidence: Defined as consistent evidence from a small number of studies.
underlying medical conditions that increase a person’s risk of severe illness from COVID-19
Level of Evidence Condition
Strongest and Most Consistent Evidence
  • Serious heart conditions, such as heart failure, coronary artery disease, or cardiomyopathies
  • Cancer
  • Chronic kidney disease
  • COPD
  • Obesity (BMI> 30)
  • Sickle cell disease
  • Solid organ transplantation
  • Type 2 diabetes mellitus
Mixed Evidence
Limited Evidence

This list is a living document that will be periodically updated, and it could rapidly change as the science evolves.

References

  1. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA; et al. (2018). "Fourth Universal Definition of Myocardial Infarction (2018)". J Am Coll Cardiol. 72 (18): 2231–2264. doi:10.1016/j.jacc.2018.08.1038. PMID 30153967.
  2. Guo T, Fan Y, Chen M, Wu X, Zhang L, He T; et al. (2020). "Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiol. doi:10.1001/jamacardio.2020.1017. PMC 7101506 Check |pmc= value (help). PMID 32219356 Check |pmid= value (help).
  3. (PDF) https://www.cdc.gov/coronavirus/2019-ncov/downloads/community-mitigation-strategy.pdf. Missing or empty |title= (help)

6/20/2020

Acute Coronary Syndromes

Pathophysiology

The mechanism of COVID-19 cardiovascular injury has not been fully understood and is likely multifactorial.

  • SARS-CoV-2 virus attaches to ACE 2 protein for ligand binding before entering the cell via receptor-mediated endocytosis.
    • Based on single-cell RNA sequencing more than 7.5% of myocardial cells have positive ACE2 expression. This protein can mediate the entry of SARS-CoV-2 and result in direct cardiotoxicity.
  • The cytokine release caused by the virus may lead to vascular inflammation, plaque instability, myocardial inflammation, a hypercoagulable state, or direct myocardial suppression.

Pathological changes:

  • In the level of cardiac tissue: minimal change to interstitial inflammatory infiltration and myocyte necrosis
  • In the level of vasculature: micro-thrombosis and vascular inflammation[1]

ST-Elevation MI (STEMI)

A US model from 9 major centers showed a 38% drop in total STEMI activations during the COVID-19 pandemic. There is a 40% reduction noted in Spain as well. there was also a delay between the first presentation to a medical encounter up to 318 min. This is important since COVID-19 can potentially be a cause of STEMI through microthrombi, cytokine storm, coronary spasm, or direct endothelial injury.[2]

  • Potential etiologies for the reduction in STEMI PPCI activations:
    • avoidance of medical care due to social distancing or concerns of contracting COVID-19 in the hospital
    • STEMI misdiagnosis
    • increased use of pharmacological reperfusion due to COVID-19

It is very important to realize if patients' anxiety is the reason behind decreasing the presentation of STEMI to U.S. hospitals.[3]

  • Treatment of STEMI & COVID-19: The specific protocols for the treatment have been evolving. Early recommendations showed intravenous thrombolysis as first-line therapy for STEMI patients with confirmed COVID-19 since most hospitals do not have protected cardiac catheterization labs.[2]

Signs and Symptoms

The signs and symptoms of acute coronary syndrome include:[4]

Treatment

In patients with ACS, and COVID-19 treatment should follow the guideline of the updated Society for Cardiovascular Angiography and Interventions guidelines.[5]


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Overview

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Pathophysiology

Causes

Differentiating Xyz from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief:

Synonyms and keywords: Novel coronavirus, covid-19, COVID-19, SARS-CoV-2, Wuhan coronavirus


Overview

  • COVID-19 patients with cardiovascular comorbidities have higher mortality.
  • Hospitalized patients with COVID-19 and Cardiovascular disease seem to be more prevalent in both the USA and China. [1]
  • In a case series with 187 patients who had confirmed COVID-19, 27.8% of patients had a myocardial injury, which caused cardiac dysfunction and arrhythmias. The result was significantly higher mortality among patients with myocardial injury.
  • It seems to be advisable to triage patients with COVID-19 based on their underlying CVD for a more aggressive treatment plan.
  • The mortality during hospitalization was shown to be 7.62% for patients without underlying CVD and normal TnT levels, 13.33% for those with underlying CVD and normal TnT levels, 37.50% for those without underlying CVD but elevated TnT levels, and 69.44% for those with underlying CVD and elevated TnTs.[6]

Historical Perspective

Classification

ST-Elevation Myocardial Infarction (STEMI)

A US model from 9 major centers showed a 38% drop in total STEMI activations during the COVID-19 pandemic. There is a 40% reduction noted in Spain as well. there was also a delay between the first presentation to a medical encounter up to 318 min. This is important since COVID-19 can potentially be a cause of STEMI through microthrombi, cytokine storm, coronary spasm, or direct endothelial injury.[2]

  • Potential etiologies for the reduction in STEMI PPCI activations:
    • avoidance of medical care due to social distancing or concerns of contracting COVID-19 in the hospital
    • STEMI misdiagnosis
    • increased use of pharmacological reperfusion due to COVID-19

It is very important to realize if patients' anxiety is the reason behind decreasing the presentation of STEMI to U.S. hospitals.[3]

  • Treatment of STEMI & COVID-19: The specific protocols for the treatment have been evolving. Early recommendations showed intravenous thrombolysis as first-line therapy for STEMI patients with confirmed COVID-19 since most hospitals do not have protected cardiac catheterization labs.[2]

Pathophysiology

The mechanism of COVID-19 cardiovascular injury has not been fully understood and is likely multifactorial.

  • SARS-CoV-2 virus attaches to ACE 2 protein for ligand binding before entering the cell via receptor-mediated endocytosis.
    • Based on single-cell RNA sequencing more than 7.5% of myocardial cells have positive ACE2 expression. This protein can mediate the entry of SARS-CoV-2 and result in direct cardiotoxicity.
  • The cytokine release caused by the virus may lead to vascular inflammation, plaque instability, myocardial inflammation, a hypercoagulable state, or direct myocardial suppression.

Pathological changes:

  • In the level of cardiac tissue: minimal change to interstitial inflammatory infiltration and myocyte necrosis
  • In the level of vasculature: micro-thrombosis and vascular inflammation[1]

Diagnosis

Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies

History and Symptoms

The signs and symptoms of acute coronary syndrome include:[4]

Treatment

Medical Therapy | Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies In patients with ACS, and COVID-19, treatment should follow the guidelines of the updated Society for Cardiovascular Angiography and Interventions.[1] [5]

History and Symptoms

Physical Examination

Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].

Treatment

In patients with ACS, and COVID-19, treatment should follow the guidelines of the updated Society for Cardiovascular Angiography and Interventions.[1] [5]

  1. 1.0 1.1 1.2 1.3 1.4 Kang Y, Chen T, Mui D, Ferrari V, Jagasia D, Scherrer-Crosbie M; et al. (2020). "Cardiovascular manifestations and treatment considerations in covid-19". Heart. doi:10.1136/heartjnl-2020-317056. PMC 7211105 Check |pmc= value (help). PMID 32354800 Check |pmid= value (help).
  2. 2.0 2.1 2.2 2.3 Ullah W, Sattar Y, Saeed R, Ahmad A, Boigon MI, Haas DC; et al. (2020). "As the COVID-19 pandemic drags on, where have all the STEMIs gone?". Int J Cardiol Heart Vasc. 29: 100550. doi:10.1016/j.ijcha.2020.100550. PMC 7261452 Check |pmc= value (help). PMID 32550258 Check |pmid= value (help).
  3. 3.0 3.1 Garcia S, Albaghdadi MS, Meraj PM, Schmidt C, Garberich R, Jaffer FA; et al. (2020). "Reduction in ST-Segment Elevation Cardiac Catheterization Laboratory Activations in the United States During COVID-19 Pandemic". J Am Coll Cardiol. 75 (22): 2871–2872. doi:10.1016/j.jacc.2020.04.011. PMC 7151384 Check |pmc= value (help). PMID 32283124 Check |pmid= value (help).
  4. 4.0 4.1 4.2 Abidov A, Rozanski A, Hachamovitch R, Hayes SW, Aboul-Enein F, Cohen I; et al. (2005). "Prognostic significance of dyspnea in patients referred for cardiac stress testing". N Engl J Med. 353 (18): 1889–98. doi:10.1056/NEJMoa042741. PMID 16267320. Review in: Evid Based Med. 2006 Jun;11(3):91
  5. 5.0 5.1 5.2 Szerlip M, Anwaruddin S, Aronow HD, Cohen MG, Daniels MJ, Dehghani P; et al. (2020). "Considerations for cardiac catheterization laboratory procedures during the COVID-19 pandemic perspectives from the Society for Cardiovascular Angiography and Interventions Emerging Leader Mentorship (SCAI ELM) Members and Graduates". Catheter Cardiovasc Interv. doi:10.1002/ccd.28887. PMID 32212409 Check |pmid= value (help).
  6. Guo T, Fan Y, Chen M, Wu X, Zhang L, He T; et al. (2020). "Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiol. doi:10.1001/jamacardio.2020.1017. PMC 7101506 Check |pmc= value (help). PMID 32219356 Check |pmid= value (help).