Microplastics and Misinformation: What Science Really Says
November 12, 2025
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Background
Around the globe, acute myocardial infarction (AMI) leads to millions of deaths every year with an annual incidence of more than 1 million cases in the United States. It can be differentiated into STEMI (ST-segment elevation myocardial infarction) and NSTEMI (non-ST-segment myocardial infarction). The heart muscle suffers from permanent injury when it does not get enough oxygen, which affects the systolic and diastolic function, raising the risk of arrythmias paving way to serious complications.
Quick restoration of blood supply to the heart is crucial and the therapy should begin within six hours of the onset of symptoms and chances for survival are best. A diagnosis scan be made based on symptoms that indicate limited blood flow, such as changes in ST segments, LBBB (left bundle branch block) or pathologic Q waves which appear on the ECG (electrocardiogram) readings taken after the occurrence of the event. Additionally, doctors may look for signs of abnormality of new regional wall motion in an imaging study along with presence of intracoronary thrombus in an angiography or autopsy.
Epidemiology
The leading cause of acute myocardial infarction is blockage resulting from atherosclerotic plaques, which accounts for about 70% of fatal cases. Given that atherosclerosis is the main reason why people have heart attacks, it becomes necessary to prevent diseases associated with it by reducing the risk factors. Men’s modifiable risk factors contribute to 90% while that of women stands at 94%. These factors include smoking tobacco products, not being physically active, having high levels of blood pressure or being obese as well as having high levels of cholesterol especially LDL (low-density lipoproteins) and triglycerides in blood. Conversely, age and sex that cannot be changed are also non-modifiable risk factors for AMI and atherosclerosis along with family history.
Anatomy
Pathophysiology
When the origin of an atherosclerotic lesion is discredited, monocytes and macrophages incite inflammation that promote blood clotting as well as the clumping together of platelets. This chain of events reduces the amount of oxygen carried through arteries to the heart muscle thus making it to not get enough oxygen. Lack of production of ATP in mitochondria due to lack of oxygen activates an ischemic cascade finally leading to cell death (apoptosis) of endocardium or MI (myocardial infarction).
Etiology
Decreased blood flow through the coronary arteries is the main cause of acute myocardial infarction. The lack of sufficient oxygen supply to the heart can be attributed to this event. There are several reasons for this to occur. For example, rupture of atherosclerotic plaque, coronary artery embolism, cocaine-induced myocardial ischemia, coronary vasospasm and coronary dissection are all possible causes. Risk factors over which individuals have no control include age, sex, family history and pattern of baldness in men. Smoking, dyslipidemia, diabetes, hypertension, poor oral hygiene, increased levels of homocysteine, sedentary lifestyle, peripheral vascular disease can be controlled. Other possible causes may include vasculitis, use of drugs like cocaine, trauma, anemia, hyperthyroidism, anomalies of coronary artery, aortic dissection and coronary artery emboli.
Genetics
Prognostic Factors
MI has a high fatality rate of 30% with most deaths occurring prior to hospitalization. Prognosis is determined by cardiac muscle injury and ejection fraction. Better outcomes result from preserved left ventricular function. Factors that can make the outlook worse include old age, diabetes, congestive heart failure, increased levels of B-type natriuretic peptides, C-reactive protein, and depression.
Clinical History
The clinical history of myocardial infarction includes risk factors such as smoking, high blood pressure, cholesterol, diabetes, obesity, and a family history of heart disease.
Symptoms of a heart attack may include chest pain or discomfort, shortness of breath, sweating, nausea or vomiting, light-headedness or dizziness, and pain or discomfort in the arms, back, neck, jaw, or stomach.
A diagnosis of myocardial infarction is typically made based on a combination of clinical symptoms, electrocardiogram (ECG) results, and blood tests that measure levels of specific proteins released during a heart attack.
Physical Examination
This includes examining for vital signs such as pulmonary evaluation, cardiac auscultation, diaphoresis etc. Examination of specific vital aspects include:
Pulses: improper pulses can be noticed in aortic dissection, that indicates a serious arterial problem.
Heart rate: Atrial fibrillation, tachycardia, or ventricular arrythmia can be observed, which is a sign of cardiac electrical disturbance.
Neck veins: Distended veins in the neck may be seen suggesting a right ventricular failure
Respiratory findings: Fever and tachypnoea indicating an inflammatory response can be seen.
Blood pressure: A typically high blood pressure is present in AMI but it can become lowered because of compromised cardiac function if the patient is in shock.
Cardiac assessments: A new mitral regurgitation murmur, apical pulse lateral displacement and a palpable S4 sound may be exhibited by the heart. Rupture of ventricular septum can be identified by a loud holosystolic murmur that radiates into the sternum.
Pulmonary evaluation: Rales and wheezing can be noticed if the patient develops pulmonary oedema which indicates the accumulation of fluid in the lungs.
Extremities: Cyanosis or edema could be observed in the extremities along with cool sensation due to lack of circulation.
Other associated symptoms include anxiety, cough, diaphoresis, wheezing, light headedness, sensation of choking, and irregular heart rate.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Emphasis on early detection and intervention must be done, in addition to the use of medicinal drugs like antiplatelet agents, anticoagulant, nitroglycerin, and oxygen therapy. Thrombolytic therapy for STEMI patients can be advised along with risk-stratification tools for high-risk patients. Changes in lifestyle, cardiac rehabilitation, drug compliance, management of risk factors as well as regular check ups also plays a crucial role.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
It is necessary for the emergency medical services (EMS) environment to have advanced cardiac life support capability, trained personnel, and calm settings. Hospitals require a triage section, cardiac care unit, and restricted entry to emergency equipment. Facilities for post-acute care need to have step-down units, rehabilitation centres, and secure living areas. Homes should be designed with open plan living spaces, medication management systems, and a supportive social network. Lifestyle adjustments must include stress reduction measures, physical exercises, public enlightenment about smoking should be carried out. Counselling services are aimed at psychosocial support among other type should be provided.
Use of anti-platelet agents
Aspirin: It must be administered to patients with AMI to reduce cardiac mortality rate by 23% in the initial month.
Clopidogrel: It selectively inhibits the binding of ADP (adenosine diphosphate) to platelet receptors and subsequent activation of glycoprotein GPIIb/IIIa complex that is ADP-mediated and further inhibits the aggregation of platelets.
Ticagrelor: This drug along with its major metabolite reversibly interacts with the P2Y12 ADP-platelet receptor and prevents the transduction of signals and platelet activation. It is advised to reduce the incidence of thrombotic cardiovascular events in those suffering with ACS (acute coronary syndrome).
Prasugrel: It is a prodrug and thienopyridine derivative which inhibits the aggregation and activation of platelets via irreversible binding of active metabolite to ADP (adenosine diphosphate) platelet receptors.
Vorapaxar: This drug reversibly inhibits the (PAR-1) protease activated receptor-1 that is present on the platelets. Due to its longer half-life the effect is made irreversible. It is also indicated in reduction of thrombotic cardiovascular events.
Use of antithrombotic agents
Bivalirudin: It is a synthetic analogue of recombinant hirudin and inhibits thrombin. It is employed as anticoagulant in patients suffering with unstable angina.
Heparin: It enhances the activity of antithrombin III preventing the conversion of fibrinogen to fibrin. It can inhibit the formation of thrombin thereby preventing reaccumulation of clot following spontaneous fibrinolysis.
Enoxaparin: It increases the inhibition of thrombin and factor Xa with increasing activity of antithrombin III. It also increases the activity of factor Xa preferentially.
Dalteparin: This enhances the inhibition of thrombin and factor Xa via increasing the activity of antithrombin III.
Use of glycoprotein IIb/IIIa inhibitors
Abciximab: It is a chimeric human-murine monoclonal antibody. It is known to bind to the platelet surface GPIIb/IIIa (glycoprotein IIb/IIIa) with high affinity thereby reducing aggregation of platelets by 80% and preventing the binding of fibrinogen.
Tirofiban: It is a non-peptide antagonist of GPIIb/IIIa receptor. It reversibly antagonizes the binding of fibrinogen and when given intravenously, platelet aggregation is inhibited by more than 90%.
Eptifibatide: This is a cyclic peptide which inhibits aggregation of platelets reversibly by binding to GPIIb/IIIa receptor.
Use of vasodilators
Nitroglycerin IV: This causes the relaxation of vascular smooth muscle by stimulating the production of intracellular cyclic guanosine monophosphate causing reduction in the blood pressure.
Use of beta-adrenergic blockers
Metoprolol: This drug potentially suppresses the ventricular ectopy because of ischemia or excessive catecholamines. In case od myocardial ischemia, beta-blockers possess antiarrhythmic effects.
Esmolol: It is particularly useful in patients who are at risk of undergoing complications due to beta-blockers particularly mild to moderate left ventricular dysfunction, reactive airway disease and peripheral vascular disease.
Atenolol: It is a selective beta-1 blocker with no or little effects on beta-2 receptors and used in treating hypertension.
Use of ACE (angiotensin-converting enzyme) inhibitors
Captopril: It is an ACE inhibitor with shorter half-life and hence used in initiation therapy.
Enalapril: This is involved in the prevention of conversion of angiotensin I to angiotensin II which is a potent vasoconstrictor. This drug helps to control proteinuria and blood pressure.
Quinapril: This drug causes an increase in the levels of renin in plasma by preventing the conversion of angiotensin I to angiotensin II.
Use of angiotensin-receptor blockers
Irbesartan: This drug blocks the aldosterone-secreting and vasoconstrictor effects angiotensin II at the receptor site.
Candesartan: It is known to block the aldosterone-secreting and vasoconstrictor effects angiotensin II at the receptor site.
Valsartan: It produces the direct antagonism of angiotensin II receptors.
Losartan: It is an antagonist of angiotensin II receptor which blocks the aldosterone-secretion and vasoconstriction effects of angiotensin II.
Use of thrombolytics
Alteplase: This is a fibrin specific agent with a half-life of five minutes. It is used as an adjunctive therapy with heparin IV to maintain the patency of arteries.
Tenecteplase: This is a modified form of alteplase which is obtained by substitution of three amino acids of alteplase. This drug causes less non intracranial bleed, but the risk of stroke and intracranial bleed is like that of alteplase.
Use of analgesics
Morphine sulfate: This is a narcotic analgesic and a drug of choice because of its safety profile, reversibility and predictable effects.
Use of PCSK9 inhibitors
Evolocumab: This is a human monoclonal IgG2 directed agent that acts against PCSK9 (proprotein convertase subtilisin/kexin type 9) and prevents the binding of circulating PCSK9 to LDLR. Levels of LDL cholesterol in the blood may be lowered by these effects.
Alirocumab: This monoclonal antibody binds to PCSK9 and lowers the levels of LDL cholesterol in the blood.
use-of-phases-of-management-in-treating-acute-myocardial-infarction
Recognition of symptoms and contacting Emergency Medical Services (EMS) if acute myocardial infarction (AMI) is suspected are the activities that constitute the pre-hospital phase. This is followed by immediate hospital management which includes rapid assessment, diagnosis through tests and initial drug therapy. Management involves reperfusion therapy using primary percutaneous coronary intervention (PCI) or thrombolytic therapy. It extends to risk stratification for high-risk patients whereas medical care tends to be conservative among low risk factors. Constant monitoring for symptoms, modification of lifestyle, management of risk factors, and psychosocial support plays a crucial role.
Medication
10
mg
Orally
every 12 hrs
10 units intravenous bolus (above 2 minutes), after that Next dose given 30 minutes after initial (for total combined dose of 20 units) Treatment should start as soon as possible after onset of acute myocardial infarction Use a separate intravenous line for each bolus injection so that no other drugs are infused or administered at the same time.
Inject, as early as possible (inside 30 minutes) after onset of acute myocardial Infarction.
30 to 50 mg intravenous bolus above 5 seconds once (based on body mass)
<60 kg: 30 mg
60 to 70 kg: 35 mg
70 to 80 kg: 40 mg
80 to 90 kg: 45 mg
>90 kg: 50 mg
Indicated to restore function for hemodialysis Catheters (Orphan)
6000 units/min into the coronary artery, infused for two hours, administered after IV heparin. Alternately, 2-3 million units of Intravenous are administered over 45-90 minutes
7.5 mg is given orally every 12 hours for 2 days, followed by 15 mg is given every 12 hours for next 2 days, and followed by 30 mg is given every 12 hours for more than 6 weeks
Administer dose of 20 mg as a bolus and then followed by dose of 60 mg infused over an hour
Do not exceed 100mg
Accelerated infusion(1-1/2 hr)-
≤67kg:
1 to 2 mins- 15mg IVP bolus
>30 mins-0.75mg/kg IV infusion
>60 mins-0.5mg/kg IV
≥67kg:
1 to 2 mins-15mg IVP bolus
>30 mins-50mg IV infusion
>60 mins-35mg IV
3-HOUR Infusion:
≤67kg:
1 to 2 mins- 0.075mg IVP bolus
>60 mins-0.675mg/kg IV infusion
>120 mins-0.25mg/kg IV
≥67kg:
1 to 2 mins-6-10mg IVP bolus
>60 mins-50-54mg IV infusion
>120 mins-20mg IV
Future Trends
Around the globe, acute myocardial infarction (AMI) leads to millions of deaths every year with an annual incidence of more than 1 million cases in the United States. It can be differentiated into STEMI (ST-segment elevation myocardial infarction) and NSTEMI (non-ST-segment myocardial infarction). The heart muscle suffers from permanent injury when it does not get enough oxygen, which affects the systolic and diastolic function, raising the risk of arrythmias paving way to serious complications.
Quick restoration of blood supply to the heart is crucial and the therapy should begin within six hours of the onset of symptoms and chances for survival are best. A diagnosis scan be made based on symptoms that indicate limited blood flow, such as changes in ST segments, LBBB (left bundle branch block) or pathologic Q waves which appear on the ECG (electrocardiogram) readings taken after the occurrence of the event. Additionally, doctors may look for signs of abnormality of new regional wall motion in an imaging study along with presence of intracoronary thrombus in an angiography or autopsy.
The leading cause of acute myocardial infarction is blockage resulting from atherosclerotic plaques, which accounts for about 70% of fatal cases. Given that atherosclerosis is the main reason why people have heart attacks, it becomes necessary to prevent diseases associated with it by reducing the risk factors. Men’s modifiable risk factors contribute to 90% while that of women stands at 94%. These factors include smoking tobacco products, not being physically active, having high levels of blood pressure or being obese as well as having high levels of cholesterol especially LDL (low-density lipoproteins) and triglycerides in blood. Conversely, age and sex that cannot be changed are also non-modifiable risk factors for AMI and atherosclerosis along with family history.
When the origin of an atherosclerotic lesion is discredited, monocytes and macrophages incite inflammation that promote blood clotting as well as the clumping together of platelets. This chain of events reduces the amount of oxygen carried through arteries to the heart muscle thus making it to not get enough oxygen. Lack of production of ATP in mitochondria due to lack of oxygen activates an ischemic cascade finally leading to cell death (apoptosis) of endocardium or MI (myocardial infarction).
Decreased blood flow through the coronary arteries is the main cause of acute myocardial infarction. The lack of sufficient oxygen supply to the heart can be attributed to this event. There are several reasons for this to occur. For example, rupture of atherosclerotic plaque, coronary artery embolism, cocaine-induced myocardial ischemia, coronary vasospasm and coronary dissection are all possible causes. Risk factors over which individuals have no control include age, sex, family history and pattern of baldness in men. Smoking, dyslipidemia, diabetes, hypertension, poor oral hygiene, increased levels of homocysteine, sedentary lifestyle, peripheral vascular disease can be controlled. Other possible causes may include vasculitis, use of drugs like cocaine, trauma, anemia, hyperthyroidism, anomalies of coronary artery, aortic dissection and coronary artery emboli.
MI has a high fatality rate of 30% with most deaths occurring prior to hospitalization. Prognosis is determined by cardiac muscle injury and ejection fraction. Better outcomes result from preserved left ventricular function. Factors that can make the outlook worse include old age, diabetes, congestive heart failure, increased levels of B-type natriuretic peptides, C-reactive protein, and depression.
The clinical history of myocardial infarction includes risk factors such as smoking, high blood pressure, cholesterol, diabetes, obesity, and a family history of heart disease.
Symptoms of a heart attack may include chest pain or discomfort, shortness of breath, sweating, nausea or vomiting, light-headedness or dizziness, and pain or discomfort in the arms, back, neck, jaw, or stomach.
A diagnosis of myocardial infarction is typically made based on a combination of clinical symptoms, electrocardiogram (ECG) results, and blood tests that measure levels of specific proteins released during a heart attack.
This includes examining for vital signs such as pulmonary evaluation, cardiac auscultation, diaphoresis etc. Examination of specific vital aspects include:
Pulses: improper pulses can be noticed in aortic dissection, that indicates a serious arterial problem.
Heart rate: Atrial fibrillation, tachycardia, or ventricular arrythmia can be observed, which is a sign of cardiac electrical disturbance.
Neck veins: Distended veins in the neck may be seen suggesting a right ventricular failure
Respiratory findings: Fever and tachypnoea indicating an inflammatory response can be seen.
Blood pressure: A typically high blood pressure is present in AMI but it can become lowered because of compromised cardiac function if the patient is in shock.
Cardiac assessments: A new mitral regurgitation murmur, apical pulse lateral displacement and a palpable S4 sound may be exhibited by the heart. Rupture of ventricular septum can be identified by a loud holosystolic murmur that radiates into the sternum.
Pulmonary evaluation: Rales and wheezing can be noticed if the patient develops pulmonary oedema which indicates the accumulation of fluid in the lungs.
Extremities: Cyanosis or edema could be observed in the extremities along with cool sensation due to lack of circulation.
Other associated symptoms include anxiety, cough, diaphoresis, wheezing, light headedness, sensation of choking, and irregular heart rate.
Emphasis on early detection and intervention must be done, in addition to the use of medicinal drugs like antiplatelet agents, anticoagulant, nitroglycerin, and oxygen therapy. Thrombolytic therapy for STEMI patients can be advised along with risk-stratification tools for high-risk patients. Changes in lifestyle, cardiac rehabilitation, drug compliance, management of risk factors as well as regular check ups also plays a crucial role.
Cardiology, General
Aspirin: It must be administered to patients with AMI to reduce cardiac mortality rate by 23% in the initial month.
Clopidogrel: It selectively inhibits the binding of ADP (adenosine diphosphate) to platelet receptors and subsequent activation of glycoprotein GPIIb/IIIa complex that is ADP-mediated and further inhibits the aggregation of platelets.
Ticagrelor: This drug along with its major metabolite reversibly interacts with the P2Y12 ADP-platelet receptor and prevents the transduction of signals and platelet activation. It is advised to reduce the incidence of thrombotic cardiovascular events in those suffering with ACS (acute coronary syndrome).
Prasugrel: It is a prodrug and thienopyridine derivative which inhibits the aggregation and activation of platelets via irreversible binding of active metabolite to ADP (adenosine diphosphate) platelet receptors.
Vorapaxar: This drug reversibly inhibits the (PAR-1) protease activated receptor-1 that is present on the platelets. Due to its longer half-life the effect is made irreversible. It is also indicated in reduction of thrombotic cardiovascular events.
Cardiology, General
Bivalirudin: It is a synthetic analogue of recombinant hirudin and inhibits thrombin. It is employed as anticoagulant in patients suffering with unstable angina.
Heparin: It enhances the activity of antithrombin III preventing the conversion of fibrinogen to fibrin. It can inhibit the formation of thrombin thereby preventing reaccumulation of clot following spontaneous fibrinolysis.
Enoxaparin: It increases the inhibition of thrombin and factor Xa with increasing activity of antithrombin III. It also increases the activity of factor Xa preferentially.
Dalteparin: This enhances the inhibition of thrombin and factor Xa via increasing the activity of antithrombin III.
Cardiology, General
Abciximab: It is a chimeric human-murine monoclonal antibody. It is known to bind to the platelet surface GPIIb/IIIa (glycoprotein IIb/IIIa) with high affinity thereby reducing aggregation of platelets by 80% and preventing the binding of fibrinogen.
Tirofiban: It is a non-peptide antagonist of GPIIb/IIIa receptor. It reversibly antagonizes the binding of fibrinogen and when given intravenously, platelet aggregation is inhibited by more than 90%.
Eptifibatide: This is a cyclic peptide which inhibits aggregation of platelets reversibly by binding to GPIIb/IIIa receptor.
Cardiology, General
Nitroglycerin IV: This causes the relaxation of vascular smooth muscle by stimulating the production of intracellular cyclic guanosine monophosphate causing reduction in the blood pressure.
Cardiology, General
Metoprolol: This drug potentially suppresses the ventricular ectopy because of ischemia or excessive catecholamines. In case od myocardial ischemia, beta-blockers possess antiarrhythmic effects.
Esmolol: It is particularly useful in patients who are at risk of undergoing complications due to beta-blockers particularly mild to moderate left ventricular dysfunction, reactive airway disease and peripheral vascular disease.
Atenolol: It is a selective beta-1 blocker with no or little effects on beta-2 receptors and used in treating hypertension.
Cardiology, General
Captopril: It is an ACE inhibitor with shorter half-life and hence used in initiation therapy.
Enalapril: This is involved in the prevention of conversion of angiotensin I to angiotensin II which is a potent vasoconstrictor. This drug helps to control proteinuria and blood pressure.
Quinapril: This drug causes an increase in the levels of renin in plasma by preventing the conversion of angiotensin I to angiotensin II.
Cardiology, General
Irbesartan: This drug blocks the aldosterone-secreting and vasoconstrictor effects angiotensin II at the receptor site.
Candesartan: It is known to block the aldosterone-secreting and vasoconstrictor effects angiotensin II at the receptor site.
Valsartan: It produces the direct antagonism of angiotensin II receptors.
Losartan: It is an antagonist of angiotensin II receptor which blocks the aldosterone-secretion and vasoconstriction effects of angiotensin II.
Cardiology, General
Alteplase: This is a fibrin specific agent with a half-life of five minutes. It is used as an adjunctive therapy with heparin IV to maintain the patency of arteries.
Tenecteplase: This is a modified form of alteplase which is obtained by substitution of three amino acids of alteplase. This drug causes less non intracranial bleed, but the risk of stroke and intracranial bleed is like that of alteplase.
Cardiology, General
Morphine sulfate: This is a narcotic analgesic and a drug of choice because of its safety profile, reversibility and predictable effects.
Cardiology, General
Evolocumab: This is a human monoclonal IgG2 directed agent that acts against PCSK9 (proprotein convertase subtilisin/kexin type 9) and prevents the binding of circulating PCSK9 to LDLR. Levels of LDL cholesterol in the blood may be lowered by these effects.
Alirocumab: This monoclonal antibody binds to PCSK9 and lowers the levels of LDL cholesterol in the blood.
Cardiology, General
Recognition of symptoms and contacting Emergency Medical Services (EMS) if acute myocardial infarction (AMI) is suspected are the activities that constitute the pre-hospital phase. This is followed by immediate hospital management which includes rapid assessment, diagnosis through tests and initial drug therapy. Management involves reperfusion therapy using primary percutaneous coronary intervention (PCI) or thrombolytic therapy. It extends to risk stratification for high-risk patients whereas medical care tends to be conservative among low risk factors. Constant monitoring for symptoms, modification of lifestyle, management of risk factors, and psychosocial support plays a crucial role.
Around the globe, acute myocardial infarction (AMI) leads to millions of deaths every year with an annual incidence of more than 1 million cases in the United States. It can be differentiated into STEMI (ST-segment elevation myocardial infarction) and NSTEMI (non-ST-segment myocardial infarction). The heart muscle suffers from permanent injury when it does not get enough oxygen, which affects the systolic and diastolic function, raising the risk of arrythmias paving way to serious complications.
Quick restoration of blood supply to the heart is crucial and the therapy should begin within six hours of the onset of symptoms and chances for survival are best. A diagnosis scan be made based on symptoms that indicate limited blood flow, such as changes in ST segments, LBBB (left bundle branch block) or pathologic Q waves which appear on the ECG (electrocardiogram) readings taken after the occurrence of the event. Additionally, doctors may look for signs of abnormality of new regional wall motion in an imaging study along with presence of intracoronary thrombus in an angiography or autopsy.
The leading cause of acute myocardial infarction is blockage resulting from atherosclerotic plaques, which accounts for about 70% of fatal cases. Given that atherosclerosis is the main reason why people have heart attacks, it becomes necessary to prevent diseases associated with it by reducing the risk factors. Men’s modifiable risk factors contribute to 90% while that of women stands at 94%. These factors include smoking tobacco products, not being physically active, having high levels of blood pressure or being obese as well as having high levels of cholesterol especially LDL (low-density lipoproteins) and triglycerides in blood. Conversely, age and sex that cannot be changed are also non-modifiable risk factors for AMI and atherosclerosis along with family history.
When the origin of an atherosclerotic lesion is discredited, monocytes and macrophages incite inflammation that promote blood clotting as well as the clumping together of platelets. This chain of events reduces the amount of oxygen carried through arteries to the heart muscle thus making it to not get enough oxygen. Lack of production of ATP in mitochondria due to lack of oxygen activates an ischemic cascade finally leading to cell death (apoptosis) of endocardium or MI (myocardial infarction).
Decreased blood flow through the coronary arteries is the main cause of acute myocardial infarction. The lack of sufficient oxygen supply to the heart can be attributed to this event. There are several reasons for this to occur. For example, rupture of atherosclerotic plaque, coronary artery embolism, cocaine-induced myocardial ischemia, coronary vasospasm and coronary dissection are all possible causes. Risk factors over which individuals have no control include age, sex, family history and pattern of baldness in men. Smoking, dyslipidemia, diabetes, hypertension, poor oral hygiene, increased levels of homocysteine, sedentary lifestyle, peripheral vascular disease can be controlled. Other possible causes may include vasculitis, use of drugs like cocaine, trauma, anemia, hyperthyroidism, anomalies of coronary artery, aortic dissection and coronary artery emboli.
MI has a high fatality rate of 30% with most deaths occurring prior to hospitalization. Prognosis is determined by cardiac muscle injury and ejection fraction. Better outcomes result from preserved left ventricular function. Factors that can make the outlook worse include old age, diabetes, congestive heart failure, increased levels of B-type natriuretic peptides, C-reactive protein, and depression.
The clinical history of myocardial infarction includes risk factors such as smoking, high blood pressure, cholesterol, diabetes, obesity, and a family history of heart disease.
Symptoms of a heart attack may include chest pain or discomfort, shortness of breath, sweating, nausea or vomiting, light-headedness or dizziness, and pain or discomfort in the arms, back, neck, jaw, or stomach.
A diagnosis of myocardial infarction is typically made based on a combination of clinical symptoms, electrocardiogram (ECG) results, and blood tests that measure levels of specific proteins released during a heart attack.
This includes examining for vital signs such as pulmonary evaluation, cardiac auscultation, diaphoresis etc. Examination of specific vital aspects include:
Pulses: improper pulses can be noticed in aortic dissection, that indicates a serious arterial problem.
Heart rate: Atrial fibrillation, tachycardia, or ventricular arrythmia can be observed, which is a sign of cardiac electrical disturbance.
Neck veins: Distended veins in the neck may be seen suggesting a right ventricular failure
Respiratory findings: Fever and tachypnoea indicating an inflammatory response can be seen.
Blood pressure: A typically high blood pressure is present in AMI but it can become lowered because of compromised cardiac function if the patient is in shock.
Cardiac assessments: A new mitral regurgitation murmur, apical pulse lateral displacement and a palpable S4 sound may be exhibited by the heart. Rupture of ventricular septum can be identified by a loud holosystolic murmur that radiates into the sternum.
Pulmonary evaluation: Rales and wheezing can be noticed if the patient develops pulmonary oedema which indicates the accumulation of fluid in the lungs.
Extremities: Cyanosis or edema could be observed in the extremities along with cool sensation due to lack of circulation.
Other associated symptoms include anxiety, cough, diaphoresis, wheezing, light headedness, sensation of choking, and irregular heart rate.
Emphasis on early detection and intervention must be done, in addition to the use of medicinal drugs like antiplatelet agents, anticoagulant, nitroglycerin, and oxygen therapy. Thrombolytic therapy for STEMI patients can be advised along with risk-stratification tools for high-risk patients. Changes in lifestyle, cardiac rehabilitation, drug compliance, management of risk factors as well as regular check ups also plays a crucial role.
Cardiology, General
It is necessary for the emergency medical services (EMS) environment to have advanced cardiac life support capability, trained personnel, and calm settings. Hospitals require a triage section, cardiac care unit, and restricted entry to emergency equipment. Facilities for post-acute care need to have step-down units, rehabilitation centres, and secure living areas. Homes should be designed with open plan living spaces, medication management systems, and a supportive social network. Lifestyle adjustments must include stress reduction measures, physical exercises, public enlightenment about smoking should be carried out. Counselling services are aimed at psychosocial support among other type should be provided.
Cardiology, General
Aspirin: It must be administered to patients with AMI to reduce cardiac mortality rate by 23% in the initial month.
Clopidogrel: It selectively inhibits the binding of ADP (adenosine diphosphate) to platelet receptors and subsequent activation of glycoprotein GPIIb/IIIa complex that is ADP-mediated and further inhibits the aggregation of platelets.
Ticagrelor: This drug along with its major metabolite reversibly interacts with the P2Y12 ADP-platelet receptor and prevents the transduction of signals and platelet activation. It is advised to reduce the incidence of thrombotic cardiovascular events in those suffering with ACS (acute coronary syndrome).
Prasugrel: It is a prodrug and thienopyridine derivative which inhibits the aggregation and activation of platelets via irreversible binding of active metabolite to ADP (adenosine diphosphate) platelet receptors.
Vorapaxar: This drug reversibly inhibits the (PAR-1) protease activated receptor-1 that is present on the platelets. Due to its longer half-life the effect is made irreversible. It is also indicated in reduction of thrombotic cardiovascular events.
Cardiology, General
Bivalirudin: It is a synthetic analogue of recombinant hirudin and inhibits thrombin. It is employed as anticoagulant in patients suffering with unstable angina.
Heparin: It enhances the activity of antithrombin III preventing the conversion of fibrinogen to fibrin. It can inhibit the formation of thrombin thereby preventing reaccumulation of clot following spontaneous fibrinolysis.
Enoxaparin: It increases the inhibition of thrombin and factor Xa with increasing activity of antithrombin III. It also increases the activity of factor Xa preferentially.
Dalteparin: This enhances the inhibition of thrombin and factor Xa via increasing the activity of antithrombin III.
Cardiology, General
Abciximab: It is a chimeric human-murine monoclonal antibody. It is known to bind to the platelet surface GPIIb/IIIa (glycoprotein IIb/IIIa) with high affinity thereby reducing aggregation of platelets by 80% and preventing the binding of fibrinogen.
Tirofiban: It is a non-peptide antagonist of GPIIb/IIIa receptor. It reversibly antagonizes the binding of fibrinogen and when given intravenously, platelet aggregation is inhibited by more than 90%.
Eptifibatide: This is a cyclic peptide which inhibits aggregation of platelets reversibly by binding to GPIIb/IIIa receptor.
Cardiology, General
Nitroglycerin IV: This causes the relaxation of vascular smooth muscle by stimulating the production of intracellular cyclic guanosine monophosphate causing reduction in the blood pressure.
Cardiology, General
Metoprolol: This drug potentially suppresses the ventricular ectopy because of ischemia or excessive catecholamines. In case od myocardial ischemia, beta-blockers possess antiarrhythmic effects.
Esmolol: It is particularly useful in patients who are at risk of undergoing complications due to beta-blockers particularly mild to moderate left ventricular dysfunction, reactive airway disease and peripheral vascular disease.
Atenolol: It is a selective beta-1 blocker with no or little effects on beta-2 receptors and used in treating hypertension.
Cardiology, General
Captopril: It is an ACE inhibitor with shorter half-life and hence used in initiation therapy.
Enalapril: This is involved in the prevention of conversion of angiotensin I to angiotensin II which is a potent vasoconstrictor. This drug helps to control proteinuria and blood pressure.
Quinapril: This drug causes an increase in the levels of renin in plasma by preventing the conversion of angiotensin I to angiotensin II.
Cardiology, General
Irbesartan: This drug blocks the aldosterone-secreting and vasoconstrictor effects angiotensin II at the receptor site.
Candesartan: It is known to block the aldosterone-secreting and vasoconstrictor effects angiotensin II at the receptor site.
Valsartan: It produces the direct antagonism of angiotensin II receptors.
Losartan: It is an antagonist of angiotensin II receptor which blocks the aldosterone-secretion and vasoconstriction effects of angiotensin II.
Cardiology, General
Alteplase: This is a fibrin specific agent with a half-life of five minutes. It is used as an adjunctive therapy with heparin IV to maintain the patency of arteries.
Tenecteplase: This is a modified form of alteplase which is obtained by substitution of three amino acids of alteplase. This drug causes less non intracranial bleed, but the risk of stroke and intracranial bleed is like that of alteplase.
Cardiology, General
Morphine sulfate: This is a narcotic analgesic and a drug of choice because of its safety profile, reversibility and predictable effects.
Cardiology, General
Evolocumab: This is a human monoclonal IgG2 directed agent that acts against PCSK9 (proprotein convertase subtilisin/kexin type 9) and prevents the binding of circulating PCSK9 to LDLR. Levels of LDL cholesterol in the blood may be lowered by these effects.
Alirocumab: This monoclonal antibody binds to PCSK9 and lowers the levels of LDL cholesterol in the blood.
Cardiology, General
Recognition of symptoms and contacting Emergency Medical Services (EMS) if acute myocardial infarction (AMI) is suspected are the activities that constitute the pre-hospital phase. This is followed by immediate hospital management which includes rapid assessment, diagnosis through tests and initial drug therapy. Management involves reperfusion therapy using primary percutaneous coronary intervention (PCI) or thrombolytic therapy. It extends to risk stratification for high-risk patients whereas medical care tends to be conservative among low risk factors. Constant monitoring for symptoms, modification of lifestyle, management of risk factors, and psychosocial support plays a crucial role.
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