Hypotension
—Rapid volume loading with an IV infusion should be administered to patients without clinical evidence for volume overload.
According to the haemocrit values saline/colloid solutions or blood to optimum LV filling pressures. (as high as 18 mm of Hg in cases of acute MI) can be used.
— Rhythm disturbances or conduction abnormalities causing hypotension should be corrected(see arrhythmias).
— Intra aortic balloon pulsation (IABP) should be inserted in patients who do not respond to other interventions. This helps in reducing afterload, and improve coronary perfusion.
— Ionotropic agents like dopamine, dobutamine should be started as indicated. Always rule out drug induced and mechanical complications.
a) Left Ventricular Failure
The immediate goals include adequate oxygenation, sedation and preload reduction to relieve pulmonary congestion.If LVF is associated with elevated blood pressure, medications to lower blood pressure should be started judiciously. Shortacting ACE inhibitors like captopril and IV nitrates can be started.
If LVF is not associated with elevation systemic blood pressure, impending cardiogenic shock must be suspected and treated aggressively.
b)Cardiogenic ShockEarly and prompt recognition of this clinical situation may save lives. Mortality is as high as 60-80 per cent.
Features of cardiogenic shock:
1) Clinical evidence of hypoperfusion like cold extremities, perspiration low urine output and tachycardia
2) Systolic blood pressure < 80-90 mm of Hg
3) LVEDP eH18 mm of Hg
4) PCWP eH 18 mm of Hg
5) Cardiac Index dH 1.8 L/mt/m2
Recognition of this clinical situation warrants invasive monitoring. Intervention should be performed as soon as possible. Early revasculariation, either PCI or CABG is recommended for patients less than 75 yrs old. Fibrinolytic therapy should be administered in patients not suitable for interventions stabilization of the patient with cardiogenic shock using mechanical circulatory arrest devices, such as intraaortic balloon pump is recommended. Therapeutic objective, is to establish and maintain systemic blood pressure. Judicious use of morphine and maintenance of adequate oxygenation using mechanical ventilation if necessary.The cornerstone of therapy are inotropic and vasopressor agents. Dopamine is the drug of choice.If high doses of dopamine are necessary to maintain adequate perfusion, a change to norepinephrine infusion may be considered. Dobutamine is preferred if systolic blood pressure is 90mmHg or more.
Dopamine starting dose 3 μg/kg/mt upto 20 μg/kg/ mt.
Dobutamine 2.5 μg/kg/mt upto 30 μg/kg/mt.
Norepineprrine 2-10 μg/minute as infusion.
Right Ventricular Infarction
Right ventricular infarction should be considered in all cases of acute inferior myocardial infarction, especially in the setting of low cardiac output.
A typical presentation would include
— Inferior myocardial infarction.
— Clear lung field.
— Jugular venous distension which increases on inspiration (Kussmaul’s sign).
Treatment
The major objectives in treating RV infarction are to:
1) Maintain RV preload (IV normal saline 1-2 litres).
2) Provide inotropic support.
3) Reduce RV afterload. (Judicious use of vasodilators).
4) Achieve early reperfusion – by early thrombolysis or PCI.
5) Maintain AV synchromy in case of high-grade AV block.
6) Concomitant LV dysfunction should be treated:— Avoid venodilators such as nitrates.
— Diuretic should be used with extreme caution.
Arrhythmias
According to the haemocrit values saline/colloid solutions or blood to optimum LV filling pressures. (as high as 18 mm of Hg in cases of acute MI) can be used.
— Rhythm disturbances or conduction abnormalities causing hypotension should be corrected(see arrhythmias).
— Intra aortic balloon pulsation (IABP) should be inserted in patients who do not respond to other interventions. This helps in reducing afterload, and improve coronary perfusion.
— Ionotropic agents like dopamine, dobutamine should be started as indicated. Always rule out drug induced and mechanical complications.
a) Left Ventricular Failure
The immediate goals include adequate oxygenation, sedation and preload reduction to relieve pulmonary congestion.If LVF is associated with elevated blood pressure, medications to lower blood pressure should be started judiciously. Shortacting ACE inhibitors like captopril and IV nitrates can be started.
If LVF is not associated with elevation systemic blood pressure, impending cardiogenic shock must be suspected and treated aggressively.
b)Cardiogenic ShockEarly and prompt recognition of this clinical situation may save lives. Mortality is as high as 60-80 per cent.
Features of cardiogenic shock:
1) Clinical evidence of hypoperfusion like cold extremities, perspiration low urine output and tachycardia
2) Systolic blood pressure < 80-90 mm of Hg
3) LVEDP eH18 mm of Hg
4) PCWP eH 18 mm of Hg
5) Cardiac Index dH 1.8 L/mt/m2
Recognition of this clinical situation warrants invasive monitoring. Intervention should be performed as soon as possible. Early revasculariation, either PCI or CABG is recommended for patients less than 75 yrs old. Fibrinolytic therapy should be administered in patients not suitable for interventions stabilization of the patient with cardiogenic shock using mechanical circulatory arrest devices, such as intraaortic balloon pump is recommended. Therapeutic objective, is to establish and maintain systemic blood pressure. Judicious use of morphine and maintenance of adequate oxygenation using mechanical ventilation if necessary.The cornerstone of therapy are inotropic and vasopressor agents. Dopamine is the drug of choice.If high doses of dopamine are necessary to maintain adequate perfusion, a change to norepinephrine infusion may be considered. Dobutamine is preferred if systolic blood pressure is 90mmHg or more.
Dopamine starting dose 3 μg/kg/mt upto 20 μg/kg/ mt.
Dobutamine 2.5 μg/kg/mt upto 30 μg/kg/mt.
Norepineprrine 2-10 μg/minute as infusion.
Right Ventricular Infarction
Right ventricular infarction should be considered in all cases of acute inferior myocardial infarction, especially in the setting of low cardiac output.
A typical presentation would include
— Inferior myocardial infarction.
— Clear lung field.
— Jugular venous distension which increases on inspiration (Kussmaul’s sign).
Treatment
The major objectives in treating RV infarction are to:
1) Maintain RV preload (IV normal saline 1-2 litres).
2) Provide inotropic support.
3) Reduce RV afterload. (Judicious use of vasodilators).
4) Achieve early reperfusion – by early thrombolysis or PCI.
5) Maintain AV synchromy in case of high-grade AV block.
6) Concomitant LV dysfunction should be treated:— Avoid venodilators such as nitrates.
— Diuretic should be used with extreme caution.
Arrhythmias
Both bradyarrhythmias and tachyarrhythmias pose significant problems during early phases of AMI.
Bradyarrhythmias
1)Sinus Bradycardia
Treatment is indicated if there is haemodynamic compromise. Atropine IV 0.3-0.6 mg every 3-10 mts with a total dose not exceeding 2 mg. If bradycardia persists despite atropine, electrical pacing is indicated. Isoproterenol should be avoided.
2)Atrioventricular (AV) Blocks
a)First degree AV Block
Incidence of 1st degree AV block in acute myocardial infarction MI is less than 15 per cent. Location of block is usually above his bundle. Associated bifascicular block may indicate infrahisian block.Aviod drugs like Beta-blockers, Calcium antagonist and Digoxin if PR interval is > 240 ms or if there is associated haemodymanic compromise or high degree block.
b) Second Degree AV Block
First and type I second degree AV blocks do not appear to affect survival. They are most commonly associated with occlusion of right coronary artery and are caused by ischaemia of the AV node.
i)Mobitz type 1 AV block
Occurs in upto 10 per cent of patients with acute myocardial infarction (AMI). Site of block generally occurs within the AV mode. It is usually transient and does not require specific therapy.ii)
Mobitz type II AV block
It is rare. Incidence is < 1 per cent. It is usually infrahisian. More common with anterior myocardial infarction and reflects trifascicular block. It has worse prognosis because of its potential for progression to complete heart block. Hence it is an indication for temporary transvenous or external pacemaker.
c)Complete AV Block
Occurs in about 5 per cent of patients with AMI and can occur in patients with either anterior or more commonly with inferior infarction. Prognosis depends on the anatomical location of the block.CHB in patients with inferior wall infarction usually results from intranodal or supranodal lesion and develops gradually. The escape rhythm is usually stable, with a rate exceeding 40 beats/mt, and a narrow QRS in 70 per cent of cases. Temporary pacing should be done if haemodynamically unstable. This is often transient and resolves within a few days. If it does not resolve, rarely it may require permanent pacing (PPI), as per physicians discretion. The mortality may approach 15 per cent, but associated Right Ventricular MI (RVMI) doubles the mortality.
In patients with anterior infarction CHB often occurs suddenly, 12-24 hrs after the onset of infarction. Such patients have unstable escape rhythms with wide QRS complexesand rates less than 40 beats/mt. Mortality is extremely high and approximately 70-80 per cent. Hence ventricular or AV sequential pacing is indicated in essentially all patients with Anterior Myocardial Infarction with Complete Heart Block.
3) Intraventricular Conduction Disturbances (IVCD)
The development of BBB or fascicular block during AMI usually signifies an extensive infarct.Presence of BBB identifies patients who are more likely to develop congestive heart failure, high-grade heart block or an episode of ventricular fibrillation. So mortality is high.
1)Sinus Bradycardia
Treatment is indicated if there is haemodynamic compromise. Atropine IV 0.3-0.6 mg every 3-10 mts with a total dose not exceeding 2 mg. If bradycardia persists despite atropine, electrical pacing is indicated. Isoproterenol should be avoided.
2)Atrioventricular (AV) Blocks
a)First degree AV Block
Incidence of 1st degree AV block in acute myocardial infarction MI is less than 15 per cent. Location of block is usually above his bundle. Associated bifascicular block may indicate infrahisian block.Aviod drugs like Beta-blockers, Calcium antagonist and Digoxin if PR interval is > 240 ms or if there is associated haemodymanic compromise or high degree block.
b) Second Degree AV Block
First and type I second degree AV blocks do not appear to affect survival. They are most commonly associated with occlusion of right coronary artery and are caused by ischaemia of the AV node.
i)Mobitz type 1 AV block
Occurs in upto 10 per cent of patients with acute myocardial infarction (AMI). Site of block generally occurs within the AV mode. It is usually transient and does not require specific therapy.ii)
Mobitz type II AV block
It is rare. Incidence is < 1 per cent. It is usually infrahisian. More common with anterior myocardial infarction and reflects trifascicular block. It has worse prognosis because of its potential for progression to complete heart block. Hence it is an indication for temporary transvenous or external pacemaker.
c)Complete AV Block
Occurs in about 5 per cent of patients with AMI and can occur in patients with either anterior or more commonly with inferior infarction. Prognosis depends on the anatomical location of the block.CHB in patients with inferior wall infarction usually results from intranodal or supranodal lesion and develops gradually. The escape rhythm is usually stable, with a rate exceeding 40 beats/mt, and a narrow QRS in 70 per cent of cases. Temporary pacing should be done if haemodynamically unstable. This is often transient and resolves within a few days. If it does not resolve, rarely it may require permanent pacing (PPI), as per physicians discretion. The mortality may approach 15 per cent, but associated Right Ventricular MI (RVMI) doubles the mortality.
In patients with anterior infarction CHB often occurs suddenly, 12-24 hrs after the onset of infarction. Such patients have unstable escape rhythms with wide QRS complexesand rates less than 40 beats/mt. Mortality is extremely high and approximately 70-80 per cent. Hence ventricular or AV sequential pacing is indicated in essentially all patients with Anterior Myocardial Infarction with Complete Heart Block.
3) Intraventricular Conduction Disturbances (IVCD)
The development of BBB or fascicular block during AMI usually signifies an extensive infarct.Presence of BBB identifies patients who are more likely to develop congestive heart failure, high-grade heart block or an episode of ventricular fibrillation. So mortality is high.
a)Isolated left anterior fascicular block
—This occurs in 3-5 per cent of patients with AMI. This is unlikely to progress into CHB.
b) Left posterior fascicular block
c)This occurs in 1-2 per cent of patients. The posterior fascicle is larger than the anterior fascicle, and a larger infarct is required to block it. So mortality is markedly increased.
RBBB
—This occurs in 3-5 per cent of patients with AMI. This is unlikely to progress into CHB.
b) Left posterior fascicular block
c)This occurs in 1-2 per cent of patients. The posterior fascicle is larger than the anterior fascicle, and a larger infarct is required to block it. So mortality is markedly increased.
RBBB
—This defect alone occurs in approximately 2 per cent of patients and frequently leads to AV block. This is associated with increased mortality. This has high incidence of ventricular fibrillation later and also CHF.
d) Bifascicular block—
e)This is associated with high mortality because of the occurrence of extensive
myocardial necrosis.
Asystole
—This has been reported to occur in 1-14 per cent of patients. In case of documented asystole immediate transvenous pacing is indicated. Because of the predominance of ventricular fibrillation as the cause of cardiac arrest in this setting, initial therapy include electrical cardioversion.
Indications for Permanent Pacing for Bradyarrhythmias in AMI
1) Persistent second–degree AV block in the His-Purknije system with bilateral bundle branch block or third degree AV block within or below the His-Purknije system.
2) Transient advanced second or third degree infra nodal AV block and associated bundle– branch block.
3) Persistent and symptomatic second or third degree AV block.
Pacing for persistent second or third degree AV block at AV node level.All patients who have an indication for permanent pacing after STEMI should be evaluated for implantable cardioverter defrillator which is found to be of benefit in patients who have VT or haemodynamically unstable VT and patients with associated LV dysfunction.
Tachyarrhythmias
Ventricular Premature Beats
Treatment of isolated VPBs, Couplets and non-sustained VT is not recommended unless they lead to haemodynamic compromise.
Accelerated Idioventricular Rhythm (AIVR)
Commonly defined as ventricular rhythm with a rate of 60-125 beats/min frequently called as slow ventricular tachycardia. This occurs in 20 per cent of patients. It is often observed shortly after reperfusion. Antiarrhythmic therapy is not indicated for this situation. In rare circumstances where treatment is neccesary Ca or Na channel blocking agents can be used.
Ventricular Tachycardia
Episodes of sustained ventricular tachycardia during first 48 hrs following AMI are often polymorphic and are associated with a hospital mortality of about 20 per cent. Cardioversion is always indicated for episodes of sustained haemodynamically compromising VT. Initially treated with unsynchronized electric shock with 200 joules, if unsuccessful, a second shock of 200-300 J should be given and if necessary a third shock of 360 joules.
Other Measures
1) Aggressive attempts to reduce myocardial ischaemia.
2) Beta-blockers — IV Metoprolol/Atenolol followed by oral maintenance as 3. mentioned earlier.
3) IABP if necessary.
4) Emergency revascularisation.
5) Normalization of S Potassium to > 4.5 mg/l and magnesium > 2 mg/l.
Episodes of sustained monomorphic VT associated with angina, pulmonary oedema, hypotension should be treated with synchronized electric shock of 100 J. Increasing energies may be used if not successful.Sustained monomorphic VT not associated with angina, pulmonary oedema or hypotension should be treated with:
i)Amiodarone 150 mg infused over 10 minutes (or 5 mg/kg); repeat 150 mg every 10-15 mts as needed.Or 360 mg over 6 hrs (1mg/mt), then 540 mg over next 18 hrs (0.5 mg/mt).
ii)Synchronized electrical cardioversion starting at 50 joules.
Ventricular Fibrillation
This is the most important cause of sudden cardiac death following AMI. Primary ventricular fibrillation occurs within 12 hrs of AMI. Its incidence is now much lower than it was several decades ago (< 5 per cent). Secondary ventricular fibrillation is often the final event of a progressive downhill course with left ventricular failure and cardiogenic shock. It has poor prognosis with in hospital mortality rates of 40-60 per cent. Late ventricular fibrillation develops more than 48 hrs following AMI. It usually occurs in patients with large infarcts and ventricular dysfunction.
Management
— Unsynchronized electric shock with an initial monophasic shock energy of 200 J, if unsuccessful, a second shock of 200-300 J should be given and then if necessary, a third shock of 360 J.
— Successful interruption of ventricular fibrillation or prevention of recurrent episodes may also be facilitated by administration of amiodarone.
— Electrolyte imbalance should be corrected (K to be kept > 4 mg/L and magnesium > 2 mg/dl).
PSVT
This arrhythmia occurs in < 10 per cent patients with AMI. Needs aggressive management because of its rapid rate.
1) Carotid sinus massage.
2) IV adenosine (6 mg IV over 1-2 secs, if no response, 12 mg IV after 1-2 mts may be given, repeat 12 mg if needed).
3) IV metoprolol (2.5 mg-5 mg every 2-5mts to a total of 15 mg over 10-15mts).
4) IV diltiazem (20 mg [0.25 mg/kg] over 2 mts followed by an infusion ofmg/hr).
5)IV Digoxin.
Atrial Flutter and Fibrillation
Atrial flutter is the least common arrhythmia in AMI. Occurrence is < 5 per cent. Atrial fibrillation is more common occurring in 10-15 per cent of patients with AMI. It is usually observed in patients with left ventricular failure. Other causes are pericarditis, atrial infarction or right ventricular infarction. Atrial fibrillation during AMI is associated with increased mortality and stroke particularly in patients with anterior wall infarction.
d) Bifascicular block—
e)This is associated with high mortality because of the occurrence of extensive
myocardial necrosis.
Asystole
—This has been reported to occur in 1-14 per cent of patients. In case of documented asystole immediate transvenous pacing is indicated. Because of the predominance of ventricular fibrillation as the cause of cardiac arrest in this setting, initial therapy include electrical cardioversion.
Indications for Permanent Pacing for Bradyarrhythmias in AMI
1) Persistent second–degree AV block in the His-Purknije system with bilateral bundle branch block or third degree AV block within or below the His-Purknije system.
2) Transient advanced second or third degree infra nodal AV block and associated bundle– branch block.
3) Persistent and symptomatic second or third degree AV block.
Pacing for persistent second or third degree AV block at AV node level.All patients who have an indication for permanent pacing after STEMI should be evaluated for implantable cardioverter defrillator which is found to be of benefit in patients who have VT or haemodynamically unstable VT and patients with associated LV dysfunction.
Tachyarrhythmias
Ventricular Premature Beats
Treatment of isolated VPBs, Couplets and non-sustained VT is not recommended unless they lead to haemodynamic compromise.
Accelerated Idioventricular Rhythm (AIVR)
Commonly defined as ventricular rhythm with a rate of 60-125 beats/min frequently called as slow ventricular tachycardia. This occurs in 20 per cent of patients. It is often observed shortly after reperfusion. Antiarrhythmic therapy is not indicated for this situation. In rare circumstances where treatment is neccesary Ca or Na channel blocking agents can be used.
Ventricular Tachycardia
Episodes of sustained ventricular tachycardia during first 48 hrs following AMI are often polymorphic and are associated with a hospital mortality of about 20 per cent. Cardioversion is always indicated for episodes of sustained haemodynamically compromising VT. Initially treated with unsynchronized electric shock with 200 joules, if unsuccessful, a second shock of 200-300 J should be given and if necessary a third shock of 360 joules.
Other Measures
1) Aggressive attempts to reduce myocardial ischaemia.
2) Beta-blockers — IV Metoprolol/Atenolol followed by oral maintenance as 3. mentioned earlier.
3) IABP if necessary.
4) Emergency revascularisation.
5) Normalization of S Potassium to > 4.5 mg/l and magnesium > 2 mg/l.
Episodes of sustained monomorphic VT associated with angina, pulmonary oedema, hypotension should be treated with synchronized electric shock of 100 J. Increasing energies may be used if not successful.Sustained monomorphic VT not associated with angina, pulmonary oedema or hypotension should be treated with:
i)Amiodarone 150 mg infused over 10 minutes (or 5 mg/kg); repeat 150 mg every 10-15 mts as needed.Or 360 mg over 6 hrs (1mg/mt), then 540 mg over next 18 hrs (0.5 mg/mt).
ii)Synchronized electrical cardioversion starting at 50 joules.
Ventricular Fibrillation
This is the most important cause of sudden cardiac death following AMI. Primary ventricular fibrillation occurs within 12 hrs of AMI. Its incidence is now much lower than it was several decades ago (< 5 per cent). Secondary ventricular fibrillation is often the final event of a progressive downhill course with left ventricular failure and cardiogenic shock. It has poor prognosis with in hospital mortality rates of 40-60 per cent. Late ventricular fibrillation develops more than 48 hrs following AMI. It usually occurs in patients with large infarcts and ventricular dysfunction.
Management
— Unsynchronized electric shock with an initial monophasic shock energy of 200 J, if unsuccessful, a second shock of 200-300 J should be given and then if necessary, a third shock of 360 J.
— Successful interruption of ventricular fibrillation or prevention of recurrent episodes may also be facilitated by administration of amiodarone.
— Electrolyte imbalance should be corrected (K to be kept > 4 mg/L and magnesium > 2 mg/dl).
PSVT
This arrhythmia occurs in < 10 per cent patients with AMI. Needs aggressive management because of its rapid rate.
1) Carotid sinus massage.
2) IV adenosine (6 mg IV over 1-2 secs, if no response, 12 mg IV after 1-2 mts may be given, repeat 12 mg if needed).
3) IV metoprolol (2.5 mg-5 mg every 2-5mts to a total of 15 mg over 10-15mts).
4) IV diltiazem (20 mg [0.25 mg/kg] over 2 mts followed by an infusion ofmg/hr).
5)IV Digoxin.
Atrial Flutter and Fibrillation
Atrial flutter is the least common arrhythmia in AMI. Occurrence is < 5 per cent. Atrial fibrillation is more common occurring in 10-15 per cent of patients with AMI. It is usually observed in patients with left ventricular failure. Other causes are pericarditis, atrial infarction or right ventricular infarction. Atrial fibrillation during AMI is associated with increased mortality and stroke particularly in patients with anterior wall infarction.
Indication of Implantable Cardiocurter Defibrillator in AMI Patients
1) Patients with AMI who had VF or haemodynamically unstable VT more than 2 days after STEMI, provided the arrhythmia is not due to transient or reversible ischaemia or reinfarction.
2) An ICD is also indicated in patients in whom a spontaneous VT or VF occurs atleast a month after AMI and who have an LVEF of 30 – 40 per cent. A nonsustained VT or inducible VF on electrophysiological testing are additional pointers for ICD implantation.
Mechanical Complications
Papillary Muscle Rupture
Rupture of papillary muscle occurs in approximately 1 per cent of MI and usually occurs 2-7 days after the infarction. Patients presents with sudden onset of pulmonary oedema. Examination reveals a mid to holosystolic murmur. Although murmur is generally loud, a thrill is rarely present. Diagnosis can be confirmed by echocardiogram. The postreomedial papillary muscle is involved 6-12 times more frequently than antero lateral papillary muscles. So papillary muscle rupture with an acute anterior MI is uncommon. Prognosis is poor, so immediate recognition and surgical treatment should be considered.
Ventricular Septal Rupture
Rupture of IVS is estimated to occur in 1-3 per cent of AMI. Ventricular septal rupture occurs with an approximately equal frequency in anterior and inferior infarctions. Majority occur in thefirst week 20-30 per cent may develop as early as 24 hrs after infarction. Patient presents with sudden clinical deterioration. Clinical evaluation reveal new systolic murmur along the left sternal border often associated with a thrill, features of pulmonary and systemic venous congestion. Signs of systemic venous congestion will be out of proportion to those of pulmonary venous congestive due to RV volume overload due to the shunt. The diagnosis can be established by echocardiography. Right heart catherisation is useful in confirming the situation.
Cardiac Rupture
Occurs in up to 24 per cent of fatal AMIs. After cardiogenic shock and arrhythmias, it is the most common cause of death. The free wall of the ventricle is the most common site of rupture. It generally occurs in the 1st – 2nd week of infarction. Free wall rupture is more likely to occur with the initial myocardial infarction, in women, in the 6th decade of life or later and in patients with
hypertension particularly if there is no hypertrophy.Presents as sudden unanticipated cardiac death.
Secondary Prevention
Secondary prevention therapies are an essential part of the management of all patients with ischaemic heart disease.
1)Patient Education Before Discharge
Before hospital discharge, all patients should be educated about life style changes and drug therapies that are important for the secondary prevention. Strict control of blood pressure and diabetic status is a must.
2)Weight Management
Desirable body mass index is 185-24.9 kg/m2. A waist circumference greater than 40 inches in men and 35 inches in women needs in evaluation for metabolic syndrome and implimentation of weight reduction strategies.
3)Smoking
Smoking has multiple cardiovascular effects that can promote AMI, including enhanced platelet aggregation, coronary vasospasm, and vascular inflammation. Complete abstinence from smoking is an essential goal after AMI.
4)Physical Activity
Encourage minimum of 30-60 mts of activity, preferably daily or at least 3-4 times weekly.
5)Lipid Management
a)Diet: Diet low in saturated fat and cholesterol (less than 7 per cent of total calories as saturated fat and less than 200gm/d cholesterol) should be started after recovery from AMI.
b) Drug therapy: The target LDL-C level post MI should be substantially less than 100 mg/dl.
Additional drug therapy should be instituted according to the following guide.
—LDL-C substantially less than 100 mg/dl (baseline or on treatment) Continue therapy.— LDL-C greater than or equal to 100 mg/dl (baseline or on treatment)
— Intensify LDL-C lowering therapy with drug treatment, giving preference to statins.
If TG is 200 mg/dl or greater. Non HDL-C should be substantially lower than 130 mg/dl.
—If TG is e”150 mg/d or HDL-C is < 40 mg/dl.Emphasize weight management and physical activity, after LDL-C lowering therapy.
Consider adding fibrate or niacin.
—If TG is e” 500 mmg/dl.
Consider fibrate or niacin before LDL-C lowering.
Consider omega – 3 fatty acids as adjunct for high TG.
6)Antiplatelets
Aspirin should be continued indefinitely 75-162 mg/dl if not contraindicated. Consider clopidogrel 75 mg or warfarin if aspirin is contraindicated.
7)Betablockers
The benefits of Beta-blockers therapy for secondary prevention are well established. It should be started as early as possible post MI and continued indefinitely.
8)Renin-Angiotension-Aldosterone System Blockers
ACE inhibitors are started in all post STEMI patients, start early in stable high-risk patients (anterior MI, previous MI, Killip class > II, LVEF < 0.40)ARB’s are indicated in patients who are intolerant of ACE inhibitors and who have either clinical or radiological signs of HF or LVEF < 0.40.Aldosterone blockage is indicated in post MI patients with LVEF d” 0.40 and have either diabetes or heart failure. It is contraindicated in patients with significant renal dysfunction or hyperkalernia (K > 5.0).
1) Patients with AMI who had VF or haemodynamically unstable VT more than 2 days after STEMI, provided the arrhythmia is not due to transient or reversible ischaemia or reinfarction.
2) An ICD is also indicated in patients in whom a spontaneous VT or VF occurs atleast a month after AMI and who have an LVEF of 30 – 40 per cent. A nonsustained VT or inducible VF on electrophysiological testing are additional pointers for ICD implantation.
Mechanical Complications
Papillary Muscle Rupture
Rupture of papillary muscle occurs in approximately 1 per cent of MI and usually occurs 2-7 days after the infarction. Patients presents with sudden onset of pulmonary oedema. Examination reveals a mid to holosystolic murmur. Although murmur is generally loud, a thrill is rarely present. Diagnosis can be confirmed by echocardiogram. The postreomedial papillary muscle is involved 6-12 times more frequently than antero lateral papillary muscles. So papillary muscle rupture with an acute anterior MI is uncommon. Prognosis is poor, so immediate recognition and surgical treatment should be considered.
Ventricular Septal Rupture
Rupture of IVS is estimated to occur in 1-3 per cent of AMI. Ventricular septal rupture occurs with an approximately equal frequency in anterior and inferior infarctions. Majority occur in thefirst week 20-30 per cent may develop as early as 24 hrs after infarction. Patient presents with sudden clinical deterioration. Clinical evaluation reveal new systolic murmur along the left sternal border often associated with a thrill, features of pulmonary and systemic venous congestion. Signs of systemic venous congestion will be out of proportion to those of pulmonary venous congestive due to RV volume overload due to the shunt. The diagnosis can be established by echocardiography. Right heart catherisation is useful in confirming the situation.
Cardiac Rupture
Occurs in up to 24 per cent of fatal AMIs. After cardiogenic shock and arrhythmias, it is the most common cause of death. The free wall of the ventricle is the most common site of rupture. It generally occurs in the 1st – 2nd week of infarction. Free wall rupture is more likely to occur with the initial myocardial infarction, in women, in the 6th decade of life or later and in patients with
hypertension particularly if there is no hypertrophy.Presents as sudden unanticipated cardiac death.
Secondary Prevention
Secondary prevention therapies are an essential part of the management of all patients with ischaemic heart disease.
1)Patient Education Before Discharge
Before hospital discharge, all patients should be educated about life style changes and drug therapies that are important for the secondary prevention. Strict control of blood pressure and diabetic status is a must.
2)Weight Management
Desirable body mass index is 185-24.9 kg/m2. A waist circumference greater than 40 inches in men and 35 inches in women needs in evaluation for metabolic syndrome and implimentation of weight reduction strategies.
3)Smoking
Smoking has multiple cardiovascular effects that can promote AMI, including enhanced platelet aggregation, coronary vasospasm, and vascular inflammation. Complete abstinence from smoking is an essential goal after AMI.
4)Physical Activity
Encourage minimum of 30-60 mts of activity, preferably daily or at least 3-4 times weekly.
5)Lipid Management
a)Diet: Diet low in saturated fat and cholesterol (less than 7 per cent of total calories as saturated fat and less than 200gm/d cholesterol) should be started after recovery from AMI.
b) Drug therapy: The target LDL-C level post MI should be substantially less than 100 mg/dl.
Additional drug therapy should be instituted according to the following guide.
—LDL-C substantially less than 100 mg/dl (baseline or on treatment) Continue therapy.— LDL-C greater than or equal to 100 mg/dl (baseline or on treatment)
— Intensify LDL-C lowering therapy with drug treatment, giving preference to statins.
If TG is 200 mg/dl or greater. Non HDL-C should be substantially lower than 130 mg/dl.
—If TG is e”150 mg/d or HDL-C is < 40 mg/dl.Emphasize weight management and physical activity, after LDL-C lowering therapy.
Consider adding fibrate or niacin.
—If TG is e” 500 mmg/dl.
Consider fibrate or niacin before LDL-C lowering.
Consider omega – 3 fatty acids as adjunct for high TG.
6)Antiplatelets
Aspirin should be continued indefinitely 75-162 mg/dl if not contraindicated. Consider clopidogrel 75 mg or warfarin if aspirin is contraindicated.
7)Betablockers
The benefits of Beta-blockers therapy for secondary prevention are well established. It should be started as early as possible post MI and continued indefinitely.
8)Renin-Angiotension-Aldosterone System Blockers
ACE inhibitors are started in all post STEMI patients, start early in stable high-risk patients (anterior MI, previous MI, Killip class > II, LVEF < 0.40)ARB’s are indicated in patients who are intolerant of ACE inhibitors and who have either clinical or radiological signs of HF or LVEF < 0.40.Aldosterone blockage is indicated in post MI patients with LVEF d” 0.40 and have either diabetes or heart failure. It is contraindicated in patients with significant renal dysfunction or hyperkalernia (K > 5.0).
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