Ischemic Heart Disease Ppt.pptx 4k4q42

ISCHEMIC HEART DISEASE

Presenter: Dr. Mounika : Dr. Jayapal Rao MD,HOD,Dept of Pathology

ISCHEMIC HEART DISEASE

PLAN OF STUDY 1. 2. 3. 4. 5. 6. 7.

Need for study Definition Risk factors Pathogenesis Effects of Ischemia Angina MI

8.Investigations 9. Complications 10.DD 11.Management 12. Conclusion 13. Homoeopathic approach 14. Bibliography

Need for study • EPIDEMOLOGY: • IHD causes more deaths and disability and incurs greater economic costs than any other illness in the developed world. IHD is the single most important cause of premature death in developed world. It is serious, chronic, life-threatening illness.

• With urbanization in the developing world, the prevalence of risk factors for IHD is increasing rapidly in these regions such that a majority of the global burden of IHD is now occurring in low-income and middle-income countries. Population subgroups that appear to be particularly affected are men in South Asian countries, especially India.

Speciality of cardiac muscle? • No fatigue? • No tetanus?

Blood supply The two coronary arteries, left and right, arise from the left and right sinus of Valsalva, respectively. In 10% of individuals the circulation is considered as "left dominant" as the circumflex artery gives off the posterior descending artery. In 90%, the circulation is right dominant as the posterior interventricular artery is given off from the right coronary artery

Supply to heart occurs during Systole or Diastole?

Factors that maintain circulation • • • • • •

Pumping action of heart Elastic recoil of the arteries\ Pressure gradient Respiration Muscular exercise Effect of gravity

Factors regulating nutrition & action of heart • • • • •

O2 supply Blood pressure Temperature Inorganic ions Neuroharmones

Factors influencing coronary circulation • • • •

Mean aortic pressure Cardiac output Metabolic factors O2 supply

Conduction & nerve supply • Autorhythmic • Sympathetic & parasympathetic

DEFINITION OF IHD • The World Health Organisation has defined ischaemic heart disease (IHD) as myocardial impairment due to imbalance between coronary blood flow and myocardial requirements. • The most common cause of IHD is atherosclerotic coronary artery disease[CAD]

Aetiology MAJOR RISK FACTORS • CONSTITUTIONAL • Age • Sex • Genetic • Familial

• • • • •

Acquired Hyperlipidaemia Hypertension DM Smoking

Minor risk factors • • • • • • • •

Environmental influences Obesity Infections Harmones Physical inactivity Stressful life Role of alcohol Homocystinuria

PATHOPHYSIOLOGY OF MYOCARDIAL ISCHAEMIA Myocardial ischaemia occurs as a result of imbalance between O2 supply and demand.

Etiopathogenesis 1.Coronary atherosclerosis: • Distribution:[ SVD, TVD] • Location.

• 2. Superadded changes in coronary atherosclerosis: • Acute changes • coronary artery thrombosis • platelet aggregation

3.Non atherosclerotic causes: • Vasospasm, • Arteritis • Embolism • Trauma • Aneurysm • Compression.

Effects of Myocardial Ischemia: Depending on suddenness of onset , Duration, Degree, Location, Extent of area affected by ischemia. • • • • •

Asymptomatic state Angina pectoris Acute myocardial infarction Chronic ischemic heart disease Sudden cardiac death

ANGINA • It is derived from the greek word STRANGULATION. • It is a syndrome “SENSE OF BAND AROUND CHEST”. Patient presses his sternum with clenched fist to locate the pain. • Progressive constriction of coronary arteries cardiac pain called angina.

The types of angina include • 1. Stable angina, • 2. Unstable angina, • 3. Prinzmetal’s angina • 4. Post infarction angina

Stable angina or effort angina • Also called Heberdeen’s angina, it occurs on known physical effort, and is relieved with rest, standing or sublingual nitroglycerine. Modalities • Temperature, • Emotions,

• Diurnal • Even sometimes smoking, sexual act, shaving, straining at stool

Some cases pain is absent , Anginaequivalent symptoms breathlessness, fatigue, symptoms of decreased cardiac output.

Variants: • Start-up or Walk- through angina, • Nocturnal angina, • Decubitius angina, • Post Prandal angina, • Ammunition factories.

Class

New York Heart Association Functional Classification

Canadian Cardiovascular Society Functional Classification

I 

Patients have cardiac disease but without  the resulting limitations of physical activity.  Ordinary physical activity does not cause  undue fatigue, palpitation, dyspnea, or  anginal pain. 

Ordinary physical activity, such  as walking and climbing stairs,  does not cause angina. Angina  present with strenuous or rapid  or prolonged exertion at work or  recreation. 

II 

Patients have cardiac disease resulting in  Slight limitation of ordinary  slight limitation of physical activity. They are  activity. Walking or climbing  comfortable at rest. Ordinary physical  stairs rapidly, walking uphill,  activity results in fatigue, palpitation,  walking or stair climbing after  dyspnea, or anginal pain.  meals, in cold, or when under  emotional stress or only during  the few hours after awakening. 

III 

Patients have cardiac disease resulting  Marked limitation of  in marked limitation of physical activity.  ordinary physical activity.  They are comfortable at rest. Less than  Walking one to two blocks  ordinary physical activity causes  on the level and climbing  fatigue, palpitation, dyspnea, or anginal  more than one flight of  pain.  stairs in normal  conditions. 

IV 

Patients have cardiac disease resulting  Inability to carry on any  in inability to carry on any physical  physical activity without  activity without discomfort. Symptoms  discomfort—anginal  of cardiac insufficiency or of the anginal  syndrome may be present  syndrome may be present even at rest.  at rest.  If any physical activity is undertaken,  discomfort is increased. 

• Physical examination in patients with angina pectoris is often normal. However, there may be indication of coronary risk factors like xanthelasma or xanthomas. Palpation may reveal thickened arteries and reduced or absent pulses as signs of generalised atherosclerosis. LV enlargement, S3 or S4 gallop.

INVESTIGATIONS • 1. X-ray chest for cardiomegaly or pulmonary congestion. 2. Lipid profile 3. Blood sugar, serum uric acid and urine examination • Electrocardiogram : In 50% of patients with angina, the resting ECG is normal between anginal episodes. During an anginal episode transient ST-T depression may be noted which disappears with rest or with sublingual nitroglycerine

Prinzmetal angina • Also called variant angina, it was described by Prinzmetal in 1959. The pain usually occurs at rest at night or in the early morning hours. It is associated with ST elevation on the ECG, responds to sublingual nitroglycerine, and is caused by spasm of the coronary artery.

• Exercise stress testing may fail to induce ischaemic changes. The spasm can be induced by smoking, hyperventilation . The cause of spasm may be increased alpha-adrenergic activity during the early morning hours or platelet aggregation. Coronary angiography may reveal normal coronary arteries.

Unstable angina • Also called intermediate coronary syndrome and Preinfarction angina, it is a serious form of angina and needs special attention since 20% of these patients are likely to develop fatal or nonfatal myocardial infarction within 4 months. There is a higher incidence of left main coronary artery disease in these patients.

• Unstable angina includes (i) angina of recent onset (less than 60 days); (ii) stable angina with symptoms more severe in intensity, frequency or duration and more easily provoked; (iii) angina at rest; (iv) angina following myocardial infarction (within days or weeks).

• ST-T depression in the ECG is common... About 25% of these patients have coronary artery thrombosis. In the others, spasm plays an important role. Patients have associated severe coronary artery obstructive disease.

Management • Thrombolytic agents • PTCA • CABG

Post infarction angina • Some patients with myocardial infarction develop angina 2 days to 8 weeks following the acute infarction. Most patients have multivessel disease or partially recanalised coronary arteries with residual myocardial ischaemia.

MYOCARDIAL INFARCTION The area of muscle that has either zero flow or so little flow that it cannot sustain cardiac muscle function process called Infacrtion.

• Myocardial infarction is a serious complication of atherosclerotic coronary heart disease. In most patients (80-95%) it results from thrombotic occlusion of the infarct-related vessel. Myocardial ischaemia and necrosis set in within about 20-40 minutes

• This occurs as a wave-front starting from the subendocardial region and progressing to the subepicardial region. The entire process usually takes 6 hours to complete. Therefore any intervention for limiting infarct size should be initiated in this "time window" of 6 hours.

Etiopathogenesis: Mechanism of Myocardial ischemia: Diminished coronary blood flow, Increased myocardial demand, Hypertrophy of heart without increase in coronary blood flow.

• Infarcts may be transmural versus subendocardial infarcts: Transmural most common type 95%. Subendocardial infarct genesis is due to reduced coronary perfusion without critical stenosis

Transmural • Full thickness • Superimposed thrombus in atherosclerosis • Focal damage

Sub-endocardial • Inner 1/3 to half of ventricular wall • Decreased circulating blood volume( shock, Hypotension, Lysed thrombus) • Circumferential

Types of infarcts: • 1. Acc to anatomical region of left ventricle: Anterior, lateral, septal, circumferential or combinations. • 2. Acc to degree of thickness : Transmural, Subendocardial. • 3. Acc to age old, new [ healed & fresh].

Location of infarcts: Infarcts are most frequently located in left ventricle . Right ventricle is less susceptible to infarction due to its thin wall less metabolic requirement.

3 common regions of MI: • 1. Stenosis of left anterior descending coronary artery is most common[40% to 50%] • 2. Stenosis of right coronary artery[30% to 40%] • 3. Stenosis of left circumflex coronary artery[ 15% to 20%]

Morphology[ Pathological changes] light microscopy • First 0-6hrs- Streching of fibres. • 6-12hrs after MI – Coagulative necrosis & neutrophils begins • Up to 3 days = Coagulative necrosis, neutrophils • 1-2 weeks = Granulation tissue • ≥ 3 weeks = fine scar • ≥ 2 months = dense scar

CLINICAL FEATURES • The presenting symptoms vary from severe pain in the chest to minimal symptoms with the disease being unrecognised. In most patients, there is substernal pain of varying intensity, radiating to the arms, jaws or back or the epigastric region, with sweating. The pain lasts for 20 minutes or more and is unrelieved or partially relieved by sublingual nitroglycerine

• The discomfort may be felt as compression of chest or a burning sensation, associated with anxiety and feeling of impending death. Continuing discomfort is a symptom of ongoing ischaemia and evolving infarction. As the infarction is completed, the pain may subside completely..

• In 15-30% of patients the infarction may go un recognised because of absence of typical symptoms. About 5% of such patients have silent infarction. This is common in diabetics and elderly patients. In others, breathlessness as in acute left ventricular failure, syncope, giddiness, fatigue, abdominal pain, nausea and vomiting and unexplained hypotension may be the presenting manifestation

C/F • • • • • • •

Pain Indigestion Apprehension Shock Oliguria Low grade fever Acute pulmonary oedema

• Physical examination reveals a pale patient who is sweating, restless, in agony due to pain, and tossing in the bed in an attempt to get relief. The pulse may be rapid or slow, and regular or irregular. Bradycardia may be a prominent feature in the early hours especially in those with inferior wall infarction

Blood pressure may be normal, low or high. Auscultation may reveal S3 or S4 gallop. Paradoxical splitting of the second heart sound may be made out. Right ventricular infarction may result in increased jugular venous pressure and signs of right heart failure.

Cardiac reserve • Maximum amount of cardiac output that can increase above normal. It is 400% blood per min more than body requires.

Coronary steal syndrome • The degree of cellular death = degree of ischemia x degree of metabolism of heart . [ Increase exertion – Increase metabolism- decrease blood supply to ischemic areas leaving the blood through coronary vessels.]

INVESTIGATIONS • Leucocytosis with polymorphonuclear reaction and high ESR due to tissue necrosis are present during the first week.

• Electrocardiographic changes : The earliest changes are ST elevation occurring with the onset of chest pain. Q waves appear when transmural infarction occurs. ST segment changes start reversing early (within 24 hours or so) and T waves begin to get inverted.).

• Anterior wall infarction is diagnosed by changes in leads V1 to V4, • Lateral by changes in L1, aVL, V5 and V6, and • Inferior wall infarction by changes in L2, L3 and aVF • Posterior wall LV infarction is diagnosed by ST depression, upright T wave and tall R wave in V1 and V2.

• The initial ECG changes may be present in only about 50-75% of patients. In others, a typical history and serial serum enzyme changes provide diagnostic help. Serial ECGs improve the diagnostic yield to 85%.

• Serum enzymes: Necrosis of myocardial cells releases enzymes in the blood. • SGOT (AST) starts to rise within a few hours, reaching a peak at 24 hours and declining over the next 48-72 hours; it is not specific for cardiac muscle injury since it is present in red blood cells, liver and skeletal muscle.

• Serum creatinine phosphokinase (K) rises immediately 4 to 6hrs ; it falls to normal values within 48 hours. This enzyme is also not specific for cardiac cells and is present in skeletal muscle and brain tissue. The K isoenzyme, K-MB, is more specific for cardiac tissue; its levels have been related to the extent of myocardial infarction.

• Serum LDH levels increase late after myocardial infarction. The increase starts during the first day, peak levels are achieved during the 3rd or 4th day, and they may remain high for 14-15 days. LDH cardiac isoenzyme (LDH1) is more specific. • Troponin level is increased in AMI 4 to 6hrs and is a more sensitive indicator of myocardial neurosis high for 7 to 10 days.

MANAGEMENT Almost 30-35% of patients with AMI die due to arrhythmias, LV failure and cardiogenic shock. Half of these deaths occur in the first 1-2 hours after onset of symptoms and 70-80% in the first 24 hours. Further, the Time window for salvaging the ischaemic myocardium at risk of necrosis is about 6 hours

Reperfusion • An occluding thrombus is responsible for myocardial infarction in almost 85% of patients. It is known that the infarction is completed after several hours. An attempt should therefore be made to remove the obstruction and achieve reperfusion to reestablish blood flow to the jeopardised myocardium and so limit the size of the infarct.

Cell injury induced by free radicals, particularly reactive oxygen species, is an important mechanism of cell damage in many pathologic condition ischemia-reperfusion injury (induced by restoration of blood flow in ischemic tissue) . On perfusion excess of sodium and calcium ions due to cell membrane damage.

• For approximately 30 minutes after the onset of even the most severe ischemia, myocardial injury is potentially reversible. Thereafter, progressive loss of viability occurs that is complete by 6 to 12 hours. The benefits of reperfusion are greatest when it is achieved early, and are progressively lost when reperfusion is delayed

Ischemic Heart Disease

• Thrombolytic agents, viz. streptokinase, urokinase, acetylated streptokinase, and tPA. It achieves recanalisation in about 50% of patients, recanalisation rates are reportedly higher (75%). A major factor is the high cost of the drug.

• All thrombolytic agents should be given within 4-6 hours after the onset of chest pain. Some of the complications that can occur include reperfusion arrhythmias and bleeding. Thrombolysis is generally avoided in patients following recent operations, those with recent cerebrovascular accidents, those who have bleeding diathesis or following cardiopulmonary resuscitation.

• Thrombolytic agents help in reducing short-term mortality and improving LV function. Following thrombolytic therapy, intravenous Herapin is given for the next 24-48 hours to prevent reocclusion..

• PTCA has been used as a method of reperfusion with a success rate of 9095%.. It is a procedure of immense value in patients with cardiogenic shock, severe LV failure and large anterior myocardial infarction.

• INDICATIONS OF PTCA: • Coronary arteriography is indicated in (1) patients with chronic stable angina pectoris who are severely symptomatic despite medical therapy and who are being considered for revascularization, i.e., a percutaneous coronary intervention (PCI) or coronary artery by grafting (CABG)

• patients with troublesome symptoms that present diagnostic difficulties in whom there is a need to confirm or rule out the diagnosis of IHD.

• Coronary by surgery as a method of reperfusion is limited to patients who do not respond to thrombolytic therapy and continue to get angina and are not suitable candidates for PTCA. Complications and mortality are higher.

• Anastomosis of one or both of the internal mammary arteries or a radial artery to the coronary artery distal to the obstructive lesion is carried out. For additional obstructions that cannot be byed by an artery, a section of a vein (usually the saphenous) is used to form a connection between the aorta and the coronary artery distal to the obstructive lesion.

• Occlusion of venous grafts is observed in 10–20% of patients during the first postoperative year, in approximately 2% per year during 5- to 7-year . Long-term patency rates are considerably higher for internal mammary and radial artery implantations than saphenous vein grafts

• The survival benefit is greater in patients with abnormal LV function (ejection fraction <50%) the fraction of end diastolic volume.

Complications of Acute Myocardial Infarction • Arrhythmias • Heart failure • Cardiogenic shock • Sudden death. Rupture of interventricular septum • Thrombosis in LV causing cerebral embolism

• Rupture of ventricle into pericardial sac causing cardiac tamponade • Deep vein thrombosis in legs causing pulmonary embolism • Pericarditis during massive infarction • Aneurysm of ventricle with thrombosis and thrombo-embolic phenomenon • Dressler’s syndrome (post myocardial infarction syndrome)

Dressler’s syndrome occurs a few days to 6 weeks following myocardial infarction and is characterised by fever, Pleuropericarditis, t pains and raised ESR. It results from an autoimmune reaction to the necrosed myocardial tissue

ASYMPTOMATIC [SILENT] CORONARY ARTERY DISEASE • Several autopsy studies in accident victims or in military personnel dying in the battlefield, stress testing in asymptomatic individuals subjected to executive health check-ups, and coronary angiographic studies in individuals may have coronary artery disease without any symptoms. In many of them the first event may be sudden cardiac death or myocardial infarction.

• Some of these patients exhibit higher thresholds to electrically induced pain, others show higher endorphin levels, and still others may be diabetics with autonomic dysfunction.[ Endorphins are derived from a substance found in Pitutary gland , naturally and have pain relieving properties.]

• In addition, patients with asymptomatic ischemia after suffering a myocardial infarction are at greater risk for a second coronary event. The widespread use of exercise ECG during routine examinations has also identified some of these heretofore unrecognized patients with asymptomatic CAD

CHRONIC IHD • Ischemic Cardiomyopathy or Diffuse fibrosis in the myocardium characterstically found in elderly age group.CHF is gradually developed decompensation over a period of years • [Chronic anaemia]

SUDDEN CARDIAC DEATH AND CARDIAC ARREST • It is estimated that in 20% or more of patients with coronary artery disease, the first presenting feature may be sudden cardiac death, defined as death within few minutes to 2 hours after onset of symptoms. The usual cause is ventricular fibrillation or cardiac asystole and occasionally electromechanical dissociation.

Differential Diagnosis • 1. Pericarditis Hours to days; may be episodic Sharp Retrosternal or toward cardiac apex; may radiate to left shoulder May be relieved by sitting up and leaning forward
• Aortic dissection : Abrupt onset of unrelenting pain Tearing or ripping sensation; knifelike Anterior chest, often radiating to back, between shoulder blades.

• Pulmonary embolism: Abrupt onset; several minutes to a few hours Pleuritic Often lateral, on the side of the embolism Dyspnea, tachypnea, tachycardia, and hypotension, haemoptysis.

• Esophageal reflux -10–60 min, Burning Substernal, epigastric, Worsened by postprandial recumbency. • Relieved by antacids. • Esophageal spasm- 2–30 min ,Pressure, tightness, burning retrosternal, Can closely mimic angina,

• Peptic ulcer- Prolonged Burning Epigastric, substernal relieved with food or antacids. • Acid peptic disease: < Early mrng [ acid secretions are not neutralised by food.]

• Musculoskeletal disease- Variable, Aching < movement • May be reproduced by localized pressure on examination[ chondrosternal, costochondral .]

• Emotional and psychiatric conditions – tightness & aching; may be fleeting Variable; may be retrosternal, Situational factors may precipitate symptoms • Anxiety or depression often detectable with careful history

Prognosis Depends on: • 1.Number of diseased vessels • 2. Degree of LV dysfunction

MANAGEMENT [ADAPTATION] • Myocardial ischemia is caused by a discrepancy between the demand of the heart muscle for oxygen and the ability of the coronary circulation to meet this demand. Most patients can be helped to understand this concept and utilize it in the rational programming of activity.

• Many tasks that ordinarily evoke angina may be accomplished without symptoms simply by reducing the speed at which they are performed. Patients must appreciate the diurnal variation in their tolerance of certain activities and should reduce their energy requirements in the morning, immediately after meals, and in cold or inclement weather.

On occasion, it may be necessary to recommend a change in employment or residence to avoid physical stress. However, with the exception of manual laborers, most patients with IHD can continue to function merely by allowing more time to complete each task. In some patients, anger and frustration may be the most important factors precipitating myocardial ischemia. If these cannot be avoided, training in stress management may be useful.

• A treill exercise test to determine the approximate heart rate at which ischemic ECG changes or symptoms develop may be helpful in the development of a specific exercise program.

EXERCISES A regular program of isotonic exercise [muscles contract & there is movement] that is within the limits of each patient's threshold for the development of angina pectoris and does not exceed 80% of the heart rate associated with ischemia on exercise testing should be strongly encouraged. • Avoid Isometric exercises[muscle contract increase in tension but does not move]

CONCLUSION • Chest discomfort is one of the most common challenges for clinicians in the office or emergency department. The differential diagnosis includes conditions affecting organs throughout the thorax and abdomen, with prognostic implications that vary from benign to life-threatening.

• Failure to recognize potentially serious conditions such as acute ischemic heart disease, aortic dissection, tension pneumothorax, or pulmonary embolism can lead to serious complications, including death. Conversely, overly conservative management of low-risk patients leads to unnecessary hospital issions, tests, procedures, and anxiety. •

Homoeopathic approach • Physiological action basis said by Dr.Richard Hughes: Aconite: “In all diseases of heart characterised by increased action when leftside is chiefly involved.”[ Physiologically cardiac depressent][ Fear, anxiety, mental restlessness] Dr. Clark: Rapidity of action relieved sometimes so painful & distressing spasm

Arsenic: For incidence of cardiac cachexy. Nights are troubled by oppression and anguish. Dr. Clark: Ars.Iod: Act on heart muscle arresting degeneration & restoring vitality.

Dr. Boerick- “Same character of pain as in Angina” • Cactus: “Pain as if constricted by Iron band”[ It is a stimulant on ganglionic centres in the cardiac walls.] • Haemotoxylon: Sense of constriction is characteristic. “ Sensation as if bar lay across chest” • Lactrodectus. Mactans: Picture of Angina, constriction of chest muscles.

Hydrocyanic acid: Spasmodic constriction& tightness in chest, torturing pain in chest. • Anacardium: Also has band like sensation.

• Glonine : Nitroglycerine[ palliative non homoeopathic] • Amy.Nitrosum:For palliation in Coronary spasm.

• Tabacum: Prove the most homoeopathic drug for Angina pectoris, Constriction of heart.[ Nausea, vomiting ,death like pallor] • Camphor: As a heart stimulant for emergency use is most satisfactory remedy.[ collapse] • Veratrum: Best heart stimulant.

• Iberis:Posess efficacy in cardiac diseases.Wakes at 2 am with palpitation. • Ophidia [Naja, Bothrops][ Symptoms of thrombotic phenomena] • Craetagus: Solvent power upon crustaceous and calcareous deposits in arteries.

• Type A Personality: Aggressiveness, Competitive drive, Ambitiousness, Sense of urgency [ risk factors & modalities]. Environmental influences. Helpful in selection of remedy.

BIBLIOGRAPHY • • • •

Textbook of pathology by Dr. Harshmohan API textbook of medicine Harrisons Internal medicine. Textbook of medical physiology by Guyton

THANKYU • THANKYU