Post-infarction conduction abnormalities: Difference between revisions

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Myocardial infarction is defined as sudden ischemic death of myocardial tissue. In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque.
Myocardial infarction is defined as sudden ischemic death of myocardial tissue. In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque.
Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function.
Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function.
Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. The adult mammalian heart has negligible regenerative capacity, thus the infarcted myocardium heals through formation of a scar. Infarct healing is dependent on an inflammatory cascade, triggered by alarmins released by dying cells. Clearance of dead cells and matrix debris by infiltrating phagocytes activates anti-inflammatory pathways leading to suppression of cytokine and chemokine signaling. Activation of the renin-angiotensin-aldosterone system and release of transforming growth factor-β induce conversion of fibroblasts into myofibroblasts, promoting deposition of extracellular matrix proteins. Infarct healing is intertwined with geometric remodeling of the chamber, characterized by dilation, hypertrophy of viable segments, and progressive dysfunction. This review manuscript describes the molecular signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted heart, the mechanistic basis of the most common complications associated with myocardial infarction, and the pathophysiologic effects of established treatment strategies. Moreover, we discuss the implications of pathophysiological insights in design and implementation of new promising therapeutic approaches for patients with myocardial infarction.
Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. The adult mammalian heart has negligible regenerative capacity, thus the infarcted myocardium heals through formation of a scar. Infarct healing is dependent on an inflammatory cascade, triggered by alarmins released by dying cells. Clearance of dead cells and matrix debris by infiltrating phagocytes activates anti-inflammatory pathways leading to suppression of cytokine and chemokine signaling. Activation of the renin-angiotensin-aldosterone system and release of transforming growth factor-β induce conversion of fibroblasts into myofibroblasts, promoting deposition of extracellular matrix proteins. Infarct healing is intertwined with geometric remodeling of the chamber, characterized by dilation, hypertrophy of viable segments, and progressive dysfunction. This review manuscript describes the molecular signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted heart, the mechanistic basis of the most common complications associated with myocardial infarction, and the pathophysiologic effects of established treatment strategies. Moreover, we discuss the implications of pathophysiological insights in design and implementation of new promising therapeutic approaches for patients with myocardial infarction.<ref name="pmidPMID: 26426469">{{cite journal| author=Frangogiannis NG| title=Pathophysiology of Myocardial Infarction. | journal=Compr Physiol | year= 2015 | volume= 5 | issue= 4 | pages= 1841-75 | pmid=PMID: 26426469 | doi=10.1002/cphy.c150006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26426469  }} </ref>


==Causes==
==Causes==
Disease name] may be caused by [cause1], [cause2], or [cause3].


OR
*The usual cause of sudden blockage in a coronary artery is the formation of a blood clot (thrombus).
*most common cause of a myocardial infarction is the rupture of an atherosclerotic plaque on an artery supplying heart muscle.
*spontaneous coronary artery dissection (SCAD) and atherosclerosis as the cause of acute myocardial infarction (AMI), especially in young females.<ref name="pmidhttps://doi.org/10.1016/j.ijcard.2016.01.188">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://doi.org/10.1016/j.ijcard.2016.01.188 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }} </ref>
*A coronary artery embolism is an uncommon non-atherosclerotic cause of acute myocardial infarction.<ref name="pmidhttps://doi.org/10.1016/j.ijcard.2016.01.188">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://doi.org/10.1016/j.ijcard.2016.01.188 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }} </ref>
*Coronary occlusion secondary to vasculitis.
*Ventricular hypertrophy
*Coronary trauma.


Common causes of [disease] include [cause1], [cause2], and [cause3].
==Differentiating myocardial infarction from other Diseases==
MI must be differentiated from other diseases that cause chest pain such as :


OR
*acute pericarditis
 
*Acute Mitral Regurgitation
The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].
*myocarditis
 
*Myopericarditis
OR
*aortic stenosis
 
*aortic dissection
The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click [[Pericarditis causes#Overview|here]].
*Aortic Regurgitation
 
*Asthma
==Differentiating ((Page name)) from other Diseases==
*Anxiety Disorders
[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].
*Cardiogenic Shock
 
*pulmonary embolism
OR
*Mitral Valve Prolapse
 
*pneumonia
[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].
*pneumothorax


==Epidemiology and Demographics==
==Epidemiology and Demographics==
Line 119: Line 125:


==Risk Factors==
==Risk Factors==
There are no established risk factors for [disease name].
OR
The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].
OR
Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].


OR
*An abnormally high level of blood cholesterol (hypercholesterolemia)
*An abnormally low level of HDL (high-density lipoprotein), commonly called "good cholesterol"
*High blood pressure (hypertension)
*Diabetes
*Family history of coronary artery disease at an early age
*Cigarette smoking
*Obesity
*Physical inactivity (too little regular exercise)
*Age
Other Risk Factor:


Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
*stress
*lack of exercise
*the use of certain illegal drugs, including cocaine and amphetamines
*a history of preeclampsia, or high blood pressure during pregnancy


==Screening==
==Screening==

Latest revision as of 22:31, 26 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Parsa, MD.[2]

Synonyms and keywords:arrhythmias, ventricular septal defect, Supraventricular arrhythmias, ventricular arrhythmias, myocardial infarction, ischemic heart disease

Overview

Acute myocardial infarction (MI) remains the leading cause of mortality all over the world. Electrical conduction abnormalities commonly complicate acute myocardial infarction, leading to a further rise in long and short term morbidities and mortality rates. [1] Different types of conduction abnormalities can follow MI, with bradyarrhythmias and atrioventricular (AV) block representing the most common. Other post-MI conduction abnormalities include supraventricular arrhythmias and ventricular arrhythmias.

Historical Perspective

  • The history of myocardial infarction (MI) diagnostics has gone through a continuous evolution over the past century, when several new discoveries have contributed to remarkably increase the number of patients appropriately diagnosed with this condition.[2]
  • For the time being, acute myocardial infarction represents a history of success concerning diagnose, management and treatment, whereas it was considered a fatal disease in the beginning of the 1900s.[3]
  • The evolution of the management of acute myocardial infarction (MI) has been one of the crowning achievements of modern medicine. At the turn of the twentieth century, MI was an often-fatal condition.[4]

Classification

Bradyarrhythmia:

Atrioventricular blocks:

Bundle branch blocks:

Pathophysiology

Myocardial infarction is defined as sudden ischemic death of myocardial tissue. In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. The adult mammalian heart has negligible regenerative capacity, thus the infarcted myocardium heals through formation of a scar. Infarct healing is dependent on an inflammatory cascade, triggered by alarmins released by dying cells. Clearance of dead cells and matrix debris by infiltrating phagocytes activates anti-inflammatory pathways leading to suppression of cytokine and chemokine signaling. Activation of the renin-angiotensin-aldosterone system and release of transforming growth factor-β induce conversion of fibroblasts into myofibroblasts, promoting deposition of extracellular matrix proteins. Infarct healing is intertwined with geometric remodeling of the chamber, characterized by dilation, hypertrophy of viable segments, and progressive dysfunction. This review manuscript describes the molecular signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted heart, the mechanistic basis of the most common complications associated with myocardial infarction, and the pathophysiologic effects of established treatment strategies. Moreover, we discuss the implications of pathophysiological insights in design and implementation of new promising therapeutic approaches for patients with myocardial infarction.[5]

Causes

  • The usual cause of sudden blockage in a coronary artery is the formation of a blood clot (thrombus).
  • most common cause of a myocardial infarction is the rupture of an atherosclerotic plaque on an artery supplying heart muscle.
  • spontaneous coronary artery dissection (SCAD) and atherosclerosis as the cause of acute myocardial infarction (AMI), especially in young females.[6]
  • A coronary artery embolism is an uncommon non-atherosclerotic cause of acute myocardial infarction.[6]
  • Coronary occlusion secondary to vasculitis.
  • Ventricular hypertrophy
  • Coronary trauma.

Differentiating myocardial infarction from other Diseases

MI must be differentiated from other diseases that cause chest pain such as :

  • acute pericarditis
  • Acute Mitral Regurgitation
  • myocarditis
  • Myopericarditis
  • aortic stenosis
  • aortic dissection
  • Aortic Regurgitation
  • Asthma
  • Anxiety Disorders
  • Cardiogenic Shock
  • pulmonary embolism
  • Mitral Valve Prolapse
  • pneumonia
  • pneumothorax

Epidemiology and Demographics

The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.

OR

In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.

OR

In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate of [number range]%.


Patients of all age groups may develop [disease name].

OR

The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.

OR

[Disease name] commonly affects individuals younger than/older than [number of years] years of age.

OR

[Chronic disease name] is usually first diagnosed among [age group].

OR

[Acute disease name] commonly affects [age group].


There is no racial predilection to [disease name].

OR

[Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].


[Disease name] affects men and women equally.

OR

[Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.


The majority of [disease name] cases are reported in [geographical region].

OR

[Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].

Risk Factors

  • An abnormally high level of blood cholesterol (hypercholesterolemia)
  • An abnormally low level of HDL (high-density lipoprotein), commonly called "good cholesterol"
  • High blood pressure (hypertension)
  • Diabetes
  • Family history of coronary artery disease at an early age
  • Cigarette smoking
  • Obesity
  • Physical inactivity (too little regular exercise)
  • Age

Other Risk Factor:

  • stress
  • lack of exercise
  • the use of certain illegal drugs, including cocaine and amphetamines
  • a history of preeclampsia, or high blood pressure during pregnancy

Screening

There is insufficient evidence to recommend routine screening for [disease/malignancy].

OR

According to the [guideline name], screening for [disease name] is not recommended.

OR

According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].

Natural History, Complications, and Prognosis

If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].

OR

Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].

OR

Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.

Diagnosis

Diagnostic Study of Choice

The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].

OR

The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].

OR

The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].

OR

There are no established criteria for the diagnosis of [disease name].

History and Symptoms

The majority of patients with [disease name] are asymptomatic.

OR

The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].

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].

OR

Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

Laboratory Findings

An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].

OR

Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

OR

[Test] is usually normal among patients with [disease name].

OR

Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].

OR

There are no diagnostic laboratory findings associated with [disease name].

Electrocardiogram

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

X-ray

There are no x-ray findings associated with [disease name].

OR

An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Echocardiography or Ultrasound

There are no echocardiography/ultrasound findings associated with [disease name].

OR

Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

CT scan

There are no CT scan findings associated with [disease name].

OR

[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

MRI

There are no MRI findings associated with [disease name].

OR

[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Other Imaging Findings

There are no other imaging findings associated with [disease name].

OR

[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

There are no other diagnostic studies associated with [disease name].

OR

[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

There is no treatment for [disease name]; the mainstay of therapy is supportive care.

OR

Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].

OR

The majority of cases of [disease name] are self-limited and require only supportive care.

OR

[Disease name] is a medical emergency and requires prompt treatment.

OR

The mainstay of treatment for [disease name] is [therapy].

OR   The optimal therapy for [malignancy name] depends on the stage at diagnosis.

OR

[Therapy] is recommended among all patients who develop [disease name].

OR

Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].

OR

Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].

OR

Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].

OR

Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].

Surgery

Surgical intervention is not recommended for the management of [disease name].

OR

Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]

OR

The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].

OR

The feasibility of surgery depends on the stage of [malignancy] at diagnosis.

OR

Surgery is the mainstay of treatment for [disease or malignancy].

Primary Prevention

There are no established measures for the primary prevention of [disease name].

OR

There are no available vaccines against [disease name].

OR

Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].

OR

[Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].

Secondary Prevention

There are no established measures for the secondary prevention of [disease name].

OR

Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].

References

  1. Hashmi, Kashif Ali; Shehzad, Amir; Hashmi, Atif Ali; Khan, Amir (2018). "Atrioventricular block after acute myocardial infarction and its association with other clinical parameters in Pakistani patients: an institutional perspective". BMC Research Notes. 11 (1). doi:10.1186/s13104-018-3431-5. ISSN 1756-0500.
  2. Cervellin G, Lippi G (2014). "Of MIs and men--a historical perspective on the diagnostics of acute myocardial infarction". Semin Thromb Hemost. 40 (5): 535–43. doi:10.1055/s-0034-1383544. PMID 24967888 PMID: 24967888 Check |pmid= value (help).
  3. Teixeira R, Gonçalves L, Gersh B (2013). "Acute myocardial infarction--historical notes". Int J Cardiol. 167 (5): 1825–34. doi:10.1016/j.ijcard.2012.12.066. PMID 23340487 PMID: 23340487 Check |pmid= value (help).
  4. Smilowitz NR, Feit F (2016). "The History of Primary Angioplasty and Stenting for Acute Myocardial Infarction". Curr Cardiol Rep. 18 (1): 5. doi:10.1007/s11886-015-0681-x. PMID 26699632 PMID: 26699632 Check |pmid= value (help).
  5. Frangogiannis NG (2015). "Pathophysiology of Myocardial Infarction". Compr Physiol. 5 (4): 1841–75. doi:10.1002/cphy.c150006. PMID 26426469 PMID: 26426469 Check |pmid= value (help).
  6. 6.0 6.1 Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1016/j.ijcard.2016.01.188 Check |pmid= value (help).


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