Coronavirus disease 2019 (COVID-19)

Disease class: Coronavirus infections
Disease class: Respiratory tract infections
Disease class: Viral diseases

Disclaimer:

At the timing of writing, COVID-19 has been a known clinical entity for just over one year. 

This is an area of intense active research. 

The information presented herein is likely to change many times as new evidence is gathered and reported.

 

Causative pathogen

• Severe acute respiratory syndrome coronavirus 2
  

 

Pathophysiology

 

Clinical profile

 

History

 

See also

• Severe Acute Respiratory Syndrome (SARS)
• Middle East Respiratory Syndrome (MERS)
• Influenza
• Dengue

COVID19 Pathophysiology

Disease: Novel coronavirus disease 2019 (COVID-19)

 

This article concerns the "host side" of the infection. 

To learn more about the "viral side" (e.g. viral characteristics and virulence factors) see here: 

Severe acute respiratory syndrome coronavirus 2

 

Disclaimer:

At the timing of writing, COVID-19 has been a known clinical entity for just over one year. 

This is an area of intense active research. 

The information presented herein is likely to change many times as new evidence is gathered and reported.

 

Risk factors associated with cases of severe COVID-19:

• Advancing age
  
• Tobacco smoking
  
• Cancer
• Organ dysfunction
  
• Respiratory dysfunction
• Chronic Obstructive Pulmonary Disease
• Cystic fibrosis 
• Asthma (severe)
  
• Heart failure
• Chronic Kidney Disease 
• Chronic liver disease
• Vascular dysfunction
• Hypertension
• Cerebrovascular disease
• Endocrine/Metabolic dysfunction
• Obesity
• Type 1 Diabetes Mellitus
• Type 2 Diabetes Mellitus 
• Haemoglobinopathies
  
• Sickle cell disease
• Thalassaemia
  
• Pregnancy
  
• Immunosuppression
• Immunosuppressive therapy

 

There is evidence to suggest that a large spectrum of chronic diseases may increase the probability of severe disease and death.

• Complex metabolic derangements such as obesity and Diabetes Mellitus may cause a generalised dysfunction of immunity, predisposition to inappropriately severe inflammation, or reduced physiological reserve.
• Some pathophysiological abnormalities may interact with SARS-CoV2 directly, to cause dysfunction unique to COVID-19.
  
• Chronic organ dysfunction is associated with severe disease and death. This may result from decompensation (a vulnerable organ fails to meet rising demands during an infection). There may exist a three-way dynamic interaction between increasing organ failure (failure to meet demand), an intensifying global inflammatory response, and a rising viral load.

 

Pathological findings associated with cases of severe COVID-19:

• High blood viral load.
• Lymphocytopoenia
• Relatively low numbers of NK cells.
• Relatively low numbers of T cells.
• Monocytosis (high numbers of monocytes).
• Hypercytokinaemia
• High serum levels of NF-kB, CXCR2, CCL2, CCR2, TNF-alpha, IL-6.
• Deficiencies in interferon signalling
• Relatively low levels of Interferon-alpha
• Relatively low expression of Interferon-Stimulated Genes.

 

The findings in severe COVID-19 appear consistent with a downward spiral of rising viral load, accumulating viral-mediated tissue damage, rising inflammatory signals, accumulating host-mediated tissue damage, depleting physiological reserves, and immune exhaustion. 

Genes with variants associated with cases of severe COVID-19:

• DPP9
• Enzyme
• Healthy variant: Many potential uses. Plays a role in cell adhesion.
  
• Disease variant: Potential cell surface vulnerability for viral entry.
• IFNAR2
• Receptor
• Healthy variant: Component of interferon signalling pathway. Antiviral function.
• Disease variant: Ineffective antiviral function.
  
• TYK2
• Enzyme
• Healthy variant: Component of interferon signalling pathway. Antiviral function.
• Disease variant: Ineffective antiviral function.
  
• CCR2
• Receptor
• Healthy variant: Component of chemokine signalling pathway. Antiviral function.
• Disease variant: Ineffective antiviral function.
  
• OAS1
• Enzyme. Induced by interferon signalling.
  
• Healthy variant: Promotes viral mRNA degradation. Antiviral function.
• Disease variant: Ineffective antiviral function.
  

 

There is evidence to suggest that specific genetic vulnerabilities in a host's antiviral defences increase the probability of severe disease and death.

 

The battle against every virus

• The spread of a viral infection throughout a host's body can be imagined as a battle. A successful virus is achieving three primary goals:
• It is invading new host cells at a greater rate than the rate of virus-infected cell destruction.
  
• It is replicating at a greater rate than the rate of viral destruction.
• It is spreading to new host bodies at a greater rate than the rate of host death or viral clearance.
  
• A host who survives and clears a virus has achieved several goals:
• They identified viral-infected cells, suppressed replication, and destroyed them.
• They coordinated trafficking of immune cells to virus-infected tissues.
• They destroyed virions at a rate faster than they could replicate or spread until no active virus remained.
  
• They maintained sufficient immune function to avoid death from other infections.
• They maintained vital physiological function (e.g. metabolism, organ function).
• The hosts who are most likely to lose this battle are:
• Incapable of destroying the virus at a sufficient rate.
• Failures of a specific antiviral defence (e.g. IFNAR2) .
• Generalised immune system dysfunction (e.g. immunosuppression).
• Incapable of suppressing viral replication sufficiently. 
• Failure of a specific antiviral defence (e.g. OAS1).
  
• Incapable of vital physiological function while burdened with the infection.
• Decompensated organ failure (e.g. heart failure).
• Respiratory failure.
• Sepsis
• Septic shock
  

 

Another hypothesis

• By causing down-regulation of ACE2 receptors throughout the body, SARS-CoV2 may interact harmfully with RAAS or the kinin–kallikrein system.
  
• This may be advantageous to the virus, but it is more likely to be an unfortunate coincidence for the host.

 

Challenges in modelling COVID-19

• Severe COVID-19 is associated with a large number of factors, which can interact with each factors in many ways.
  
• This is undoubtedly a complex system. 'Complex' features include:
  
• A network of interacting components (e.g. virus-cell interactions, cytokines, metabolism, organ function).
• Feedback loops (e.g. secretion of inflammatory factors to attract cells which secrete more inflammatory factors, without resolution of the infection).
• Emergent phenomena (e.g. the impact on the function of each organ).
  
• Nonlinearity (e.g. two hosts with identical physiologies and identical risk factors may have a dramatically different course of pathophysiology on a sub-cellular, cellular, and macroscopic level)
  
• Stochastic processes (e.g. intra-host virus-cell dynamics).

 

Summary

• There is already a wealth of information available about COVID-19. Many congenital factors, and acquired factors, appear to influence the probability of severe COVID-19 and death.
• We can expect a great deal more research over the coming years. Further research should reveal synergistic or antagonistic interactions between various combinations of factors. 
• Advances in technology may facilitate predictive modelling.
  

SARS-CoV-2 VUI-202012/01

Strain of: Severe acute respiratory syndrome coronavirus 2

 Also known as:

• Lineage B.1.1.7 
• Variant Under Investigation in December 2020
  

 

Disclaimer:

At the timing of writing, COVID-19 has been a known clinical entity for just over one year. 

This is an area of intense active research. 

The information presented herein is likely to change many times as new evidence is gathered and reported.

 

Laconic

• A new strain of SARS-CoV-2 with significantly greater transmissibility.

 

Disease:

• Coronavirus Disease 2019 (COVID-19)
• Pathophysiology

 

Probable origin:

• London, United Kingdom
• September 2020
  

 

Key mutations (compared to the first SARS-CoV-2 strain)

17 in total

• N501Y : point mutation from asparagine (N) to tyrosine (Y) in amino-acid site 501

 

Clinical consequences

• Significantly increased affinity for ACE2 receptor binding.
  
• Significantly higher viral load (on average).
• Over 70% increase in transmissibility.
• No obvious increase in morbidity or mortality.
  

 

See also:

• Severe acute respiratory syndrome coronavirus 2 (First detected in China)
  
• SARS-CoV-2 Cluster 5 (First detected in Denmark)
  
• SARS-CoV-2 501.V2 Variant (First detected in South Africa)
  

COVID-19 pandemic

History of medicine: Pandemics

Disclaimer:

At the timing of writing, COVID-19 has been a known clinical entity for just over one year. 

This is an area of intense active research. 

The information presented herein is likely to change many times as new evidence is gathered and reported.

 

Causative agent:

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2)
  

 

Disease:

• Coronavirus Disease 2019 (COVID-19)

Timeline

• 1st December 2019: Patient zero experiences symptoms in Wuhan.
• Day 23: An unsolved medical case is investigated by bronchoalveolar lavage. The specimen is sent for metagenomic massive parallel sequencing analysis. 
• Day 26: SARS-CoV2 is first identified from the specimen. 
• Day 41: Chinese state media report the first death from COVID-19.
• Day 49: First confirmed case outside Wuhan, in China.
• Day 50: The Chinese state media characterises the situation as an epidemic.
• Day 50: First confirmed cases in Singapore, Malaysia, South Korea.
• Day 52: First confirmed case in North America (Washington state).
• Day 52: First confirmed case in Europe (France).
• Day 56: First confirmed case in Oceania (Australia).
• Day 57: First confirmed case in Canada.
• Day 60: First confirmed case in India.
• Day 61: First confirmed case in Russia.
• Day 62: First confirmed case in United Kingdom.
• Day 76: First confirmed case in Africa (Egypt).
• Day 87: First confirmed case in South America (Brazil).
• Day 89: First confirmed case in Mexico.
• Day 91: First confirmed case in South Africa.
• Day 93: First confirmed case in Argentina.
• Day 101: The World Health Organisation characterises the situation as a pandemic.

• Day 365: Cumulative confirmed cases in the UK = 1,617,331 (2.38%)
• Day 365: Cumulative case fatalities in the UK = 58,245 (0.10%)
• Day 365: Cumulative confirmed cases in the world = 62,411,018 (0.79%)
• Day 365: Cumulative case fatalities in the world = 1,458,118 (0.02%)

• Day 386: United Kingdom announces that strain VUI-2020/01 appears significantly more transmissible than the first strain.

 

Consequences

• Significant increase in global morbidity and mortality.
  
• Significant increase in healthcare demands, leading to oversaturation, resource depletion and preventable harm to patients.
• Millions of infections and deaths amongst healthcare workers. 
• 2020 stock market crash
• COVID-19 recession
  
• Significant decrease in revenue for many businesses.
• Mass closure of businesses.
• Significant increase in unemployment.
• Significant increase in domestic violence.
• Significant increase in social isolation and loneliness.
  
• Significant increase in prevalence and severity of depression, stress, anxiety, and other mental health disorders (e.g. schizophrenia).
• Significant increase in social inequality and poverty.
  

 

Further reading

• World Health Organisation case tracker
• Public Health England case tracker

Severe acute respiratory syndrome coronavirus

Pathogen category: (+)ssRNA viruses

Also known as

• SARS-CoV-1
• SARS virus
  

 

Pathology

• Severe Acute Respiratory Syndrome (SARS)
  

 

Features

Exploits

• ACE2 (Angiotensin Converting Enzyme 2). An cell surface enzyme. The viral spike protein has evolved a Receptor Binding Domain, with high binding affinity for ACE2.
  
• TMPRSS2 (Transmembrane protease, serine 2): A transmembrane enzyme. SARS-CoV1 and SARS-CoV2 have evolved to initiate cell entry when they interact with this enzyme on the cell surface.

 

Taxonomy

• Category: Virus     
• Realm: Riboviria
• Kingdom: Orthornavirae
• Phylum: Pisuviricota
• Class: Pisoniviricetes
• Order: Nidovirales
• Family: Coronaviridae
• Genus: Betacoronavirus
• Subgenus: Sarbecovirus
• Species: Severe acute respiratory syndrome–related coronavirus

 

See also

• Severe acute respiratory syndrome coronavirus 2 (a later strain.)
  

COVID19 Clinical profile

Disease: Novel coronavirus disease 2019 (COVID-19)

Disclaimer:

At the timing of writing, COVID-19 has been a known clinical entity for just over one year. 

This is an area of intense active research. 

The information presented herein is likely to change many times as new evidence is gathered and reported.

 

Causative pathogen

• Severe acute respiratory syndrome coronavirus 2
  

 

Symptoms

• Anosmia
• Pyrexia
• Shortness of breath
• Cough (dry)
• Chest pain
• Muscle ache
• Weakness
• Fatigue
  
• Abdominal pain
• Nausea
  
• Diarrhoea
• Confusion

 

Clinical manifestations

• Pneumonia
• Pleuritis
• Pneumonitis
• Acute Respiratory Distress Syndrome
• Delirium
• Acute Kidney Injury
• Sepsis
• Septic shock
• Pneumatosis intestinalis
• Pericarditis
• Myocarditis
• Myositis
• Enteritis
• Infarction
• Stroke
• Myocardial infarction
• Hepatitis
• Disseminated Intravascular Coagulation

Differential diagnosis includes:

• Acute heart failure
• Hypersensitivity pneumonitis
• Influenza

 

Management

• Isolation / Quarantine
• Contact tracing
  
• Nasopharyngeal swabbing and testing for viral RNA by PCR
  
• Blood tests
• Chest radiograph
• Arterial Blood Gas analysis

Interventions

• Supportive management
• Oxygen therapy 
• Continuous Positive Airway Pressure
• Prone positioning
• Intubation
• Mechanical ventilation
• Anti-coagulation therapy
• Anti-inflammatory therapy
  
• Corticosteroid treatment may reduce mortality in the population with severe disease.
• Intravenous infusions of tocilizumab OR sarilumab may reduce mortality in the population with severe disease.
• Vitamin D supplementation may reduce morbidity and mortality.
• Antibiotic therapy may help to reduce any element of opportunistic bacterial infections (e.g. viral pneumonia with secondary bacterial pneumonia).
  

 

The most deadly infectious diseases

Most deaths annually

• #1 Acute respiratory infections
• Coronavirus Disease 2019 (COVID-19)
• Influenza
• Pneumonia
• #2 AIDS (including Tuberculosis + AIDS)
• #3 Diarrhoeal diseases
• Cholera morbus 
• Norovirus gastroenteritis
  
• Rotavirus gastroenteritis
• Adenovirus gastroenteritis
• Astrovirus gastroenteritis
• Shiga-toxin producing Escherichia coli gastroenteritis
• Campylobacteriosis
• Salmonellosis
• Shigellosis
• Clostridioides difficile colitis
  
• Cryptosporidiosis
• Giardiasis
• Amoebiasis
• Blastocystosis
• Cyclosporiasis

• #4 Tuberculosis
• #5 Malaria
• #6 Measles

Highest case fatality rate

• Creutzfeldt–Jakob disease
• African trypanosomiasis
• Visceral leishmaniasis
• Primary amoebic meningoencephalitis
• Rabies
• Balamuthia
• Glanders (sepsis)
• Smallpox (malignant or haemorrhagic type)
• Ebola virus disease (Zaire ebolavirus)
• AIDS / HIV infection
• Anthrax (pulmonary)
• Macanine alphaherpesvirus 1 disease
• Aspergillosis (pulmonary) (opportunistic infection)
• Cryptococcal meningitis (co-infection with HIV)
• Influenza (H5N1)
• Plague (bubonic, pneumonic, septicaemic)
• Tularaemia (pneumonic)
• Marburg virus disease
• Tetanus
• Baylisascariasis
• Hantavirus diseases
• Middle Eastern Respiratory Syndrome
• Eastern equine encephalitis 
• Tuberculosis
  
• Varicella (in newborns)
• Dengue
• Leptospirosis
• Legionellosis
• Meningococcal diseases
• Typhoid fever
• Severe Acute Respiratory Syndrome
• Intestinal capillariasis
• Botulism
• Diphtheria
• Yellow fever
• Pertussis (in infants)
• Angiostrongyliasis
• Coronavirus Disease 2019 (COVID-19)
• Measles 
• Cholera morbus
  
• Brucellosis
• Hepatitis A
• Lassa Fever
• Mumps (encephalitis)
• Venezuelan Equine Encephalitis
• Malaria
• Polio

 

Taxonomy of most deadly diseases 

Viral diseases

• AIDS / HIV
• Coronavirus Disease 2019 (COVID-19)
• Dengue
  
• Eastern equine encephalitis 
• Ebola virus disease
• Hantavirus diseases
  
• Hepatitis A
  
• Influenza
• Lassa Fever
  
• Macanine alphaherpesvirus 1 disease 
• Marburg virus disease
• Measles
• Middle Eastern Respiratory Syndrome
  
• Mumps
  
• Polio
  
• Rabies 
• Severe Acute Respiratory Syndrome
  
• Smallpox
• Varicella 
• Venezuelan Equine Encephalitis
  
• Yellow fever
  

Bacterial diseases

• Anthrax 
• Brucellosis
• Botulism
  
• Cholera morbus 
• Diphtheria
  
• Legionellosis
• Leprosy 
• Leptospirosis
• Meningococcal diseases
  
• Paratyphoid fever 
• Pertussis
  
• Plague
• Tetanus
  
• Tuberculosis
• Tularaemia
  
• Typhoid fever
• Typhus
  

Chromistal diseases

• Blastocystosis
  
• Cryptosporidiosis
  
• Malaria

Protozoal diseases

• African trypanosomiasis
• American trypanosomiasis
• Amoebiasis 
  
• Aspergillosis (pulmonary)
• Balamuthia
  
• Giardiasis 
• Primary amoebic meningoencephalitis
• Visceral leishmaniasis

Fungal diseases

• Aspergillosis (pulmonary)
• Cryptococcal meningitis
  

Animal diseases

• Angiostrongyliasis
• Baylisascariasis
  

Prion diseases

• Creutzfeldt–Jakob disease

Severe acute respiratory syndrome coronavirus 2

Pathogen category: (+)ssRNA viruses

Also known as

• SARS-CoV-2
• 2019 novel coronavirus (2019-nCoV)

 

Disclaimer:

At the timing of writing, COVID-19 has been a known clinical entity for just over one year. 

This is an area of intense active research. 

The information presented herein is likely to change many times as new evidence is gathered and reported.

 

Pathology

• Coronavirus Disease 2019 (COVID-19)
• Pathophysiology

 

Characteristics

• SARS-CoV2 has been described by virologists as unusually proficient at suppressing the immune response until the infection is very advanced. There can be almost no signs of viral infection in tissues which are heavily burdened with compromised cells. As a result, asymptomatic carriers can spread the virus for days before they develop any signs or symptoms.
• SARS-CoV2 can survive on hard surfaces for up to 72 hours.
• Hard surfaces can be effectively cleaned with alcohol or soap solutions.
  

 

Features

Genome

• The genome is contained within a single, linear, positive-sense RNA strand.
  
• Size (# base pairs): 29,903.
  

Structural proteins

• Nucleocaspid protein (N): Houses the viral genetic material.
• Envelope (E): Forms the outermost viral envelope.
• Membrane (M): Forms the outermost viral envelope.
• Spike (S): Forms the outermost viral envelope. Binds to host cell. See 'Exploits' below.
  

Viral envelope 

• The virus is surrounded by a protective lipid (fatty) bilayer.
  

Virulence factors

• At least 3 identified. With futher research, more factors may be recognised. 
• Promote viral shedding.
• Inhibit host immune response.
• Supression of interferon signalling. 

Exploits

• ACE2 (Angiotensin Converting Enzyme 2). A cell surface enzyme. The viral spike protein has evolved a Receptor Binding Domain, with high binding affinity for ACE2.
  
• TMPRSS2 (Transmembrane protease, serine 2): A transmembrane enzyme. SARS-CoV1 and SARS-CoV2 have evolved to initiate cell entry when they interact with this enzyme on the cell surface.
  

History

 

Taxonomy

• Category: Virus     
• Realm: Riboviria
• Kingdom: Orthornavirae
• Phylum: Pisuviricota
• Class: Pisoniviricetes
• Order: Nidovirales
• Family: Coronaviridae
• Genus: Betacoronavirus
• Subgenus: Sarbecovirus
• Species: Severe acute respiratory syndrome–related coronavirus
• Strain: Severe acute respiratory syndrome coronavirus 2
  

 

See also

• SARS-CoV-2 VUI-202012/01 (A later strain. Significantly more transmissible.)
• Severe acute respiratory syndrome-related coronavirus (An earlier strain). 
• SARS-CoV-2 Cluster 5 (First detected in Denmark)
• SARS-CoV-2 501.V2 Variant (First detected in South Africa)

History of medicine: Pandemics

A pandemic is an epidemic of disease that has spread across a large region, for instance multiple continents, or worldwide.

 

Etymology

From Greek
πᾶν (pan, 'all')
δῆμος (demos, 'people' )

 

Ongoing 

• AIDS pandemic
• 2019-2020 Novel coronavirus disease 2019 (COVID-19) pandemic

 

Resolved

• The Black Death
• 1918 flu pandemic
• 1957–1958 influenza pandemic
• 1968 flu pandemic
• 2009 swine flu pandemic

 

Diseases

• Plague
• Cholera
• Typhus
• Smallpox
• Measles
• Tuberculosis
• Leprosy
• Malaria
• Yellow fever
• HIV infection
• Influenza 
• Coronavirus Disease 2019 (COVID-19)

Shigellosis

Disease class: Bacterial infection

 

This is a notifiable disease. This means that all diagnosed cases must be reported to the national Public Health services.

 

Pathogens 

• Shigella species

Measles

Disease class: Viral infection

This is a notifiable disease. This means that all diagnosed cases must be reported to the national Public Health services.

 

Also known as

• Morbilli
• Rubeola
• Red measles
• English measles

 

Pathogen

• Measles morbillivirus 

Typhoid fever

Disease class: Bacterial infection
Disease class: Salmonellosis

 

This is a notifiable disease. This means that all diagnosed cases must be reported to the national Public Health services.

 

Etymology

• Typhoid : similar to Typhus. 

 

Pathogens

• Salmonella typhi

 

Do not confuse with

• Typhus

 

See also

• Paratyphoid fever

Cocoliztli

This refers to a series of epidemics.

 

Location

• Central Mexico
• South Mexico
• South America (potentially)

 

Timeline

• 1519 : Hernando Cortés arrived in Mexico
• 1520 : Major epidemic
• 1545 : Major epidemic
• 1576 : Major epidemic
• 1736 : Major epidemic
• 1813 : Major epidemic

 

Identity

• Paratyphoid fever
• Typhus 
• Measles 
• Smallpox
• A mixed infection with multiple pathogens

 

Etymology

• The word cocoliztli originated from the Nahuatl word for "pest", or disease, illness, and plague. 

 

Death toll

• 5-18 million deaths

Paratyphoid fever

Disease class: Bacterial infection
Disease class: Salmonellosis

 

This is a notifiable disease. This means that all diagnosed cases must be reported to the national Public Health services.

 

Etymology

• Para-typhoid : Similar to Typhoid.
• Typhoid : Similar to Typhus.  

 

Pathogens

• Salmonella paratyphi

 

Do not confuse with

• Typhus

 

See also

• Typhoid fever

Smallpox

Disease class: Viral infection

 

This is a notifiable disease. This means that all diagnosed cases must be reported to the national Public Health services.

 

Also known as

• Variola
• Variola vera
• Pox
• Red plague 

 

Pathogen

• Variola virus

Plague

Disease class: Bacterial infection 

This is a notifiable disease. This means that all diagnosed cases must be reported to the national Public Health services.

 

Also known as

• The black death

 

Subtypes

• The bubonic plague
• The septicaemic plague
• The pneumonic plague

 

Pathogens

• Yersinia pestis

 

Pathophysioloy

• Yersinia pestis bacteria 'hitchhike' on immune cells in the lymph nodes and eventually ride into the lungs and the blood stream.
• Bleeding and coughing spreads the plague to new hosts.

 

History

• 430 BCE : Plague of Athens (epidemic). 
• 541 – 542 CE : Plague of Justinian (pandemic).
• 1346 – 1353 CE : The Black Death (pandemic).
• 1855 – 1912 CE : The Third Plague pandemic.
• 2019 CE : A couple died of plague in Mongolia after eating a raw kidney.

Salmonellosis

Disease class: Bacterial infection

This is a notifiable disease. This means that all diagnosed cases must be reported to the national Public Health services.

 

Subtypes

• Paratyphoid fever
• Salmonella food poisoning
• Typhoid fever

 

Pathogens 

• Salmonella species

The Black Death

Pandemic of:

• Plague

Dates:

• 1346 – 1353 CE 

 

Major features

• One of the most destructive pandemics in history. 
• Peaked in Europe from 1347 to 1351 CE.
• Approximately 33% of the European population died.
• Death toll: 75 to 200 million Eurasians.
• Total world population: Modern estimates suggest a population reduction from 450 million to between 350 - 375 million.

 

Pathogen:

• Yersinia pestis

 

Vector: 

• Fleas (carried by rodents)

CHA2DS2-VASc

Also known as

• CHADS-VASc

Calculates stroke risk for patients with atrial fibrillation, possibly better than the CHADS₂ Score.

CHA2DS2-VASc Score	Stroke Risk %	95% CI
0	0	-
1	1.3	-
2	2.2	-
3	3.2	-
4	4.0	-
5	6.7	-
6	9.8	-
7	9.6	-
8	12.5	-
9	15.2	-

C 
 Congestive heart failure (or Left ventricular systolic dysfunction)
1 H
 Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)
1 A₂
 Age ≥75 years
2 D
 Diabetes Mellitus
1 S₂
 Prior Stroke or TIA or thromboembolism
2 V
 Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)
1 A
 Age 65–74 years
1 Sc
 Sex category (i.e. female sex)
1

QRISK

Current version: QRISK3

Estimates the 10-year cardiovascular risk of an individual.

 

Prognosis

A QRISK over 10 indicates a 10% risk of CVD event over the next ten years. This indicates that primary prevention with lipid lowering therapy (such as statins) should be considered.

 

See also

• Framingham Risk Score