Cardiology Module PDF 2024-2025

Cardiology module for fourth level students (Block 7) By: Cardiology department, October 6 University 2024-2025  Table of Contents Topic Page Valvular heart diseases...

Cardiology module for fourth level students (Block 7) By: Cardiology department, October 6 University 2024-2025  Table of Contents Topic Page Valvular heart diseases 3 Infective endocarditis 14 Epidemiology of cardiovascular diseases 18 Atherosclerosis and risk factors 23 Chronic Stable Angina 26 Pharmacology (1): Antianginal and antidyslipidemic 31 Clinical pathology: Cardiac markers 36 Acute coronary syndrome (NSTEMI & STEMI) 39 Pathology of cardiovascular diseases 48 Hypertension 51 Syncope 60 Heart Failure and shock 64 Pharmacology (2): anti failure 72 Cardiomyopathies 78 Pericardial diseases 84 Aortic Dissection 88 DVT-pulmonary embolism 89 Pulmonary hypertension 94 Rate and rhythm abnormalities 96 Pharmacology (3): anti-arrhythmics 108 Cardiac surgeries 115 Revision for OSPE 119 The Head and members of Cardiology Department would like to express their deep gratitude to all the departments who collaborated in this book, namely: Pathology department, Pharmacology department, Epidemiology department, Clinical Pathology department and Cardiothoracic Surgery department.  Valvular Heart Diseases LEARNING OBJECTIVES Explain the valvular lesions pathophysiology and complications Identify the clinical signs associated with valve lesions Identify how to investigate patients with valvular heart diseases Define the methods to treat patients with valvular heart diseases Distinguish patients who will benefit from surgical treatment MITRAL STENOSIS: Mitral stenosis is the most common lesion caused by rheumatic fever. Mitral stenosis consists of thickened mitral valve leaflets, fused commissures, and chordae tendineae. Aetiology: Most cases are secondary to rheumatic fever. Rarely, it is caused by a congenital defect or calcification of the valve. Pathogenesis: see figure Figure showing pathogenesis of mitral stenosis Clinical Symptoms: Usually, manifest slowly over years. Lung congestive symptoms: Dyspnea, Orthopnea, Paroxysmal nocturnal dyspnea, Hemoptysis (due to rupture of pulmonary vessels) Palpitations and systemic embolism from AF Right-sided heart failure: hepatomegaly, ascites, peripheral edema Pressure effects (rare): Hoarseness (due to compression on the recurrent laryngeal nerve) Ortner’s syndrome 3 Physical Signs General: o Face: Malar flush o Pulse: may show Atrial fibrillation (irregular cardiac rhythm) o Lung: Pulmonary rales Local: o Inspection & palpation: o Left parasternal lift (due to right ventricular enlargement) o Slapping apex beat o Auscultation: o S1 : Loud (valve is closing from low seated position) unless valve is calcific o S2 : may be loud due to pulmonary hypertension o Opening snap (OS) following S2. OS get nearer to S2 in severe MS o Murmur: o Site: Apex (mitral area) o Timing: Mid-diastolic o Character: Rumbling (low-pitched) o Radiation: usually no radiation o Increased by: left lateral positioning and exercise N.B. The murmur can have presystolic accentuation component due to atrial contraction at the end of diastole. This is lost if AF develops. Investigations: ECG: right ventricular hypertrophy; left and right atrial abnormalities; AF Chest x-ray: o Large left atrium e.g. double-density right heart border, straightening of left heart border. o Possible signs of pulmonary congestion and hypertension, including Kerley B lines and increased vascular markings, large pulmonary artery Transthoracic Echocardiogram (most important test): (1) Confirm the diagnosis and aetiology: (2) Assess severity of stenosis: Severe M.S. = Valve area ≤ 1.5 cm2 (3) Chamber enlargement and pulmonary pressure  Figure showing ECG and CXR in mitral stenosis Treatment: 1.Medical therapy: o Reduce congestion: by Diuretics and salt-restricted diet o Control ventricular rate (give more time for left ventricular filling): by Beta blockers or non-dihydropyridine CCBs or digoxin o Anticoagulants (with warfarin) in patients with Af (Non vitamin K Oral anticoagulants should not be used in significant MS with AF) 2.Percutaneous Balloon valvotomy o Requires favorable characteristics e.g. pliable leaflets, minimal commissural fusion, and minimal calcification o Concurrent MR or left atrial thrombus is a contraindication to valvotomy 3.Surgical management: “Mitral commissurotomy or valve replacement” Timing of Intervention: Main indication: Symptoms not controlled by medications Figure showing balloon valvotomy in MS 5 MITRAL REGURGITATION: Mitral regurgitation is backflow of blood from the left ventricle into the left atrium due to inadequate functioning (insufficiency) of the mitral valve, most commonly from ischemia. The etiology of mitral regurgitation is due to abnormalities of the mitral leaflets, annulus, and chordae tendineae. In addition, abnormalities of prosthetic valves. Mitral regurge can be divided into: Acute MR and Chronic MR Figure showing difference between acute and chronic MR in pathophysiology A. Acute Mitral regurge: Causes: o Leaflets→ Acute rheumatic fever, Ischemic papillary muscle rupture o Rupture Chordae → Infective endocarditis or myxematous valve o Dilated Annulus → Acute dilation of the left ventricle e.g. myocarditis or ischemia o Mechanical failure of a prosthetic mitral valve Pathophysiology: The heart cannot accommodate the sudden large volume of blood → Acute heart failure: Acute pulmonary edema, or cardiogenic shock or even sudden cardiac death Clinical picture: Acute severe valvular regurgitation is a surgical emergency, but accurate and timely diagnosis can be difficult. The patient usually presents with acute heart failure Locally, a faint systolic murmur (due to rapid equilibrium of pressure between left atrium and left ventricle) rather than the holosystolic murmur typically heard with chronic mitral regurgitation can be heard.  Investigations: Chest x-ray in acute MR may show pulmonary edema; abnormalities in cardiac size are not evident unless an underlying chronic disorder is also present Echocardiography diagnostic and very important to be done quickly Treatment: IV Nitrate and diuretics are used to reduce the LV preload and afterload Mechanical support e.g., intra-aortic balloon pump Emergency mitral valve repair or replacement B. Chronic Mitral Regurge: Aetiology: 1. Primary MR: Due to valve abnormalities (leaflets, chordae or papillary Muscle) Common causes are mitral valve prolapse and rheumatic heart disease 2. Secondary MR: The valve leaflets and chordae are structurally normal and mitral regurgitation results from alterations in LV and LA geometry e.g. LV dilation as in heart failure (dilated annulus) Pathogenesis A portion of the left ventricular stroke volume is pumped backward into the left atrium instead of forward into the aorta, resulting in increased left atrial pressure and decreased forward cardiac output. Volume overload occurs, increasing preload. Left ventricular dysfunction occurs after years of compensation. Symptoms: Initially asymptomatic → symptoms develop as the LA enlarges, pulmonary artery pressure and venous pressure increase, and LV compensation fails. Symptoms include dyspnea, orthopnea, fatigue (due to left heart failure), and palpitations (often due to AF or volume overload). Severe and chronic mitral regurgitation lead to right-sided failure, presenting with edema, ascites, anorexia, and fatigue. Pulmonary hypertension may be a late finding. Physical Signs: General: Distended neck veins Inspection & palpation: o Hyperdynamic and displaced apex (downward and to the left) o Apical systolic thrill may be felt Auscultation: o S1 : soft o S2 : widely split, accentuated if pulmonary hypertension develop o S3 : usually heard at apex o Murmur: ▪ Site: Apical ▪ Timing: Pan systolic ▪ Character: Soft Blowing 7  ▪ Radiation: radiating to the axilla o Diastolic flow murmur over the apex (functional mitral stenosis) Main Investigations: ECG shows signs of left ventricular and left atrial enlargement. Chest x-ray shows cardiac enlargement, with pulmonary vascular congestion Echocardiography (best test): o Confirm diagnosis o Can help to determine cause e.g., MVP o Determine severity of MR, estimation of regurgitant fraction o Heart Chamber sizes o Pulmonary pressure Treatment of Severe Primary MR: Medical therapy: In Chronic MR with normal EF, there is no evidence to support prophylactic use of vasodilators such as ACE I Adequate control of BP if there is hypertension Loop diuretics are helpful in patients with exertional or nocturnal dyspnea Surgical therapy: Repair is preferable to replacement. Main Indications for surgery: o Significantly limiting symptoms despite optimal medical management. o LV fails o LV dilates o Other open-heart surgeries planned Treatment of severe secondary MR: (usually in cases of heart failure) Treated as heart failure Notes on MITRAL VALVE PROLAPSE: (MVP) It is a common congenital valvular abnormality (2–3% population) typically seen in young women. Most patients are asymptomatic, may c/o Dizziness, palpitations, syncope, and chest pain Auscultation: o Mid-to-late systolic click and a late systolic murmur at the cardiac apex o Worsens with Valsalva or standing o Improves with squatting or leg raise Complications (all very rare) o E.g. Serious arrhythmias, CHF, Acute MR , Risk of infective endocarditis Echocardiography is diagnostic and can quantify degree of MR. Treatment: o Use beta blockers for chest pain and palpitations. o Mitral valve repair/replacement is sometimes needed.  o o AORTIC STENOSIS: Causes: 1. Calcific: senile calcification of a trileaflet valve (commonest cause) 2. Congenital: calcification of a congenitally bicuspid aortic valve 3. Rheumatic: the aortic valve is affected by the rheumatic fever, the mitral valve is also invariably affected. Pathogenesis: *Aortic stenosis → Elevation of LV systolic pressure → LV hypertrophy to maintain Cardiac output (CO) without LV dilatation → Increased LV diastolic pressure → Forceful LA contraction to help the filling of the thick, noncompliant ventricle → Symptoms of pulmonary venous congestion. *Aortic stenosis → Reduced CO & forward flow → Syncopal attacks on exertion. Besides, *LVH & high intramyocardial wall tension → Increased oxygen demands & decreased diastolic coronary blood flow → Myocardial ischemia → Angina pectoris. Symptoms: (usually exertional, classic triad of symptoms) 1. Angina pectoris. 2. Syncopal attacks. 3. Dyspnea & orthopnea from CHF. N.B. Once the patient is symptomatic, life expectance is < 5 years. Examination: General : ❖ Pulsus tardus and parvus ❖ Carotid thrill Local: ❖ Inspection and palpation: ✓ Heaving sustained apex, not shifted. ✓ Palpable thrill at A1 area (Rt. Second intercostal space). ❖ Auscultation: ✓ Muffled S2 due to decreased aortic component. ✓ S4 may be heard ✓ Aortic ejection click (bicuspid valve) ✓ Murmur of AS: ▪ Timing: systolic. 9  ▪ Character: harsh ejection crescendo-decrescendo. ▪ Site & radiation: maximum intensity in A1, radiates to carotids. Main Clinical indicators of severity of AS: 1. Abnormal pulse. 2. Heaving sustained apex. 3. Decreased S2 4. Longer duration of murmur with late peaking (correlate better with severity than the intensity of the murmur). D.D. of aortic stenosis murmur Disease Differentiating Features Aortic valve sclerosis in Normal pulse. elderly No thrill & murmur isn't radiated. Functional AS murmur All signs of AR are present (occurring with AR) AS murmur not radiate to neck and no thrill HOCM Murmur starts later and does not radiate into neck Characteristic change in murmur with various maneuvers e.g. straining and standing up. Mitral regurgitation Holosystolic murmur at apex and radiates to axilla and not carotids. Carotid pulse normal and apex beat usually shifted & hyperdynamic Pulmonary stenosis Maximum intensity at the pulmonary area. Louder with inspiration. Supravalvular AS Elfin facies & hypercalcemia (as part of a syndrome). Unequal pulse volume on right & left forearms (reduced on left side). Maximum intensity on the suprasternal notch or the 1 st Rt. Space. Investigations: 1. ECG: shows left ventricular hypertrophy. 2. Chest x-ray: cardiomegaly, and pulmonary congestion. 3. Echocardiography: to confirm diagnosis, aetiology, severity and cardiac chambers. Treatment: 1. Medical treatment till intervention 2. Aortic stenosis intervention is indicated in cases of: A. Symptomatic AS. B. Presence of LV systolic dysfunction. C. Doing other valve replacement or CABG Modality of intervention: Figure showing TAVI 1. Surgical Aortic Valve Replacement: The standard management for aortic stenosis is however recently introduced transcutaneous valve replacement (TAVR) can be advised in older patients and those with high surgical risk. 2. Transcatheter Aortic Valve Implantation (TAVI) An alternative to surgical replacement in those with high surgical risk. AORTIC REGURGITATION (AR): It can result from conditions affecting the aortic valve itself or the aortic root. AR can be acute or chronic according to onset. I. Acute Aortic Regurgitation: Causes: 1. Type A Aortic Dissection (involving the ascending aorta). 2. Infective endocarditis of the aortic valve. 3. Trauma 4. Aortic Prosthetic valve malfunction Pathophysiology: The LV does not have time to dilate to accommodate the increased volume → Rapid increase in LV pressure → acute rise in pulmonary venous pressure up to Acute Pulmonary Oedema & decreased cardiac output up to Cardiogenic Shock. Symptoms: 1. Acute heart failure (dyspnea, fatigue, weakness) up to Acute Pulmonary Oedema (Acute Dyspnea & orthopnea with respiratory failure (that may need mechanical ventilation). 2. Cardiogenic shock (hypotension with resultant multisystem organ damage. Signs: 1. Peripheral signs of chronic AR are not evident 2. Muffled S2 (lack of aortic leaflet coaptation during valve closure → Reduced intensity of A2 3. Murmur of AR: usually not audible or very faint. Treatment: Acute AR requires urgent Surgical Aortic Valve Replacement or Aortic Valve Repair. II.Chronic Aortic Regurgitation: Causes: 1. Degenerative. 2. Bicuspid aortic regurgitation (These are the 2 most common aetiologies in Western countries) 3. Rheumatic heart disease. 4. Infective endocarditis. 5. Conditions affecting the ascending aorta (e.g. Marfan syndrome & ankylosing spondylitis) Pathophysiology: *Volume overload of the LV → The ventricle compensates by dilatation according to the Frank- Starling mechanism → Overstretching the myofibrils → Less actin–myosin interaction & decreased contractility. *If secondary MR occurs from dilated LV → Elevated LV diastolic pressure → pulmonary venous congestion. *Increased pulse pressure due to: 1. Increased SBP from large stroke volume. 2. Decreased DBP due to the regurgitation of blood into the left ventricle. Symptoms: Chronic aortic regurgitation is typically asymptomatic for years. 1. Dyspnea on exertion. 2. Palpitation 11 Signs: General: ▪ Peripheral signs indicating wide pulse pressure e.g. Corrigan pulse, Water hammer pulse, Duroziez sign (systolic and/or diastolic thrill or murmur heard over the femoral arteries), Hill’s sign (BP in LL higher than UL by > 60 mmHg), DeMusset’s sign (head nodding). ▪ Pulsus bisferiens. Local: 1. Apical S3 (due to dilated LV). 2. Murmur of AR: A. Timing: diastolic. B. Character: soft blowing. C. Site & radiation: maximum intensity in second aortic area, more evident if patient leans forwards & holds breath in expiration. 3. Murmur of functional aortic stenosis (on first aortic area) rdue to overflow. 4. Austin-Flint murmur is a low-pitched rumbling late-diastolic murmur heard on the apex. The diastolic murmur mimics mitral stenosis and is attributed to the effect of the AR jet on the mitral leaflet. Investigations: ▪ ECG: LV hypertrophy often with volume overload pattern ▪ Chest x-ray: LV and aortic dilation. ▪ Echocardiography: to confirm diagnosis, aetiology, severity and cardiac chambers. Treatment: ▪ Medical treatment: - ACE Is may provide symptomatic improvement in patients with chronic severe AR in whom surgery isn't feasible, but NOT recommended for patients with asymptomatic moderate or severe AR to delay surgery. - Beta blockers are recommended for patients with Marfan syndrome. ▪ Surgical Aortic Valve Replacement: indicated in severe AR if. A. Symptomatic patients. B. Decreased LV EF 50-55 mm).  Tricuspid Valve Disease: Tricuspid regurgitation: o Causes: ▪ It is usually ‘secondary’ as a result of RV or RA dilatation (commonly from left sided heart disease) ▪ Other causes include rheumatic fever, congenital diseases, carcinoid and infective endocarditis (IV drug users) and Iatrogenic causes (cardiac device implantation with a leadwire crossing through the valve). o Pathophysiology: volume overload of the RV, leading to right heart failure. o Clinically: ▪ Systemic venous congestion, including elevated JVP with giant V wave, pulsatile enlarged liver, ascites and peripheral oedema ▪ Pansystolic murmur heard at the left sternal edge that is loudest in inspiration (Carvallo sign) and associated with an RV heave. o Echocardiography is diagnostic o Management is aimed at treating the underlying cause and reducing symptoms using diuretics. Sometimes surgery is needed. Tricuspid Stenosis: o Main cause → rheumatic fever, and it is almost always accompanied by mitral or aortic valve disease. o Effect → It causes pressure overload of the RA, raising RA pressure to produce symptoms of right heart failure. o Signs → JVP is elevated with giant A waves. Local Examination reveals a mid- diastolic murmur, which is low in pitch and heard at the lower left sternal edge, loudest in inspiration. It may be associated with an opening snap. o Treatment → Diuretics, while valve replacement may be needed in symptomatic severe disease or those undergoing left sided valve surgery. 13  Infective Endocarditis LEARNING OBJECTIVES List the causes and presentation of acute and subacute infective endocarditis Recognize the microorganisms responsible for infective endocarditis Identify the risk of predisposing conditions for infective endocarditis Evaluate the methods of diagnosing infective endocarditis Identify the basis of treatment of endocarditis and indication for surgery Recognize the conditions that require prophylaxis for infective endocarditis Introduction: Infective Endocarditis (IE) is an infection of the endocardium (the inner lining of the heart chambers and valves), in which the heart valves are colonized with microbial organisms, causing friable infected vegetations and valve injury. Bacterial endocarditis produces large vegetations and may affect any valve in the heart, although left -sided lesions of the aortic and mitral valves are more common. The bacteremia can be induced by dental procedures, venous catheters, UTI and other infections, or IV drug users. Classification: Infective endocarditis could be acute or subacute: 1. Acute infective endocarditis: o It is usually caused by virulent bacteremia that may seed even in previously normal valves, leading to large, bulky vegetations o Staph. aureus is the most common cause. o Rapid onset with fever and sometimes sepsis o IV drug use a major risk factor (usually affecting tricuspid valve) o Associated with invasion of myocardium (abscess cavities) and rapid valve destruction o Embolic complications may occur, particularly to the lungs with right-sided lesions o Treatment is intensive antibiotics and usually surgery is needed 2. Subacute infective endocarditis: o It is less fatal than acute endocarditis, associated with low virulence. o It is commonly caused by viridans group streptococci. o The microbes commonly seed previously abnormal valves, producing smaller vegetations composed of fibrin, platelets, debris, and bacteria o Slow onset with vague symptoms, leading to malaise, low-grade fever, weight loss, and flu-like symptoms. o Risk factors (in the heart) include valve diseases (especially rheumatic), congenital diseases especially ventricular septal defects and prosthetic valve. o Destruction of valves is a usual sequalae and may need surgical correction. Microorganisms Responsible for Infective Endocarditis The most likely organisms for native valve endocarditis (NVE) are streptococcus viridans (more than half the cases) followed by staphylococcus aureus and other streptococci.. However, in IV addicts, most cases are caused by staphylococcal infections. Prosthetic valve endocarditis (PVE) is mostly caused by staphylococcus epidermidis in the first two months postoperatively, but late infections are similar to native valves. In summary: -Native valve → strept viridans -IV addicts → staph aureus -Early prosthetic valve endocarditis → Staph epidermidis -Late prosthetic valve endocarditis → strept viridans Complications: o CHF (most common cause of death) o Septic embolization (related to infarctions and metastatic infections): brain (“mycotic” aneurysm); spleen (greater with subacute); kidneys; coronary arteries. Right sided endocarditis can cause pulmonary abscesses o Vasculitis o Glomerulonephritis with nephrotic syndrome or renal failure (immune complex) o Cardiac extension of infection → abscess (aortic root abscess may be manifested as long PR interval in ECG) Clinical Manifestations: Symptoms are usually vague, including Fever, chills, sweating, fatigue, weight loss, dyspnea, anorexia, cough Physical signs: o General: Fever, clubbing, other signs due to vasculitis or embolic events, splenomegaly, glomerulonephritis, mycotic aneurysms o Local cardiac signs: e.g. Heart murmur (new or changing of old one) Peripheral signs of endocarditis (due to vasculitis, immune complexes or emboli): Petechiae: red, non-blanching lesions on conjunctivae, buccal mucosa, palate, extremities Splinter hemorrhages: linear, red brown streaks, usually proximal in nailbeds Osler’s nodes: 2–5 mm painful nodules on pads of fingers or toes Janeway lesions (10–15%): macular, red, or hemorrhagic, painless patches on palms or soles Roth’s spots (95% of total CK, while CK-MB is 20 mm Hg systolic suggests aortic dissection (present in ~70% of cases). o Hypotension may suggest massive pulmonary embolism or cardiac shock. o Fever may suggest pneumonia or mediastinitis (esophageal rupture) as the cause of chest pain. o Absence of pedal pulses may occur in aortic dissection Inspect and palpate the chest wall for tender areas, respiratory motion, respiratory retractions, or accessory muscle use. If the tender area corresponds to the location of the patient’s pain and palpation exactly reproduces the pain, consider musculoskeletal chest pain as the cause of chest pain. Cardiac Auscultation: Abnormal heart sounds and new murmurs e.g. o A new fourth heart sound (S4) can occur with angina or infarction. o A new murmur may be significant: ✓ Aortic regurgitation may occur in patients with aortic dissection, ✓ Mitral regurgitation can occur in patients with infarction due to papillary muscle dysfunction. The lungs should be auscultated for: o Crackles o Asymmetry of breath sounds e.g. spontaneous pneumothorax o Absent lung sounds also may occur in pneumothorax and pleural effusions. [Percussion can differentiate between Pneumothorax (Hyperresonance) and pleural effusion (stony dullness)] ECG: All patients with chest pain should have a 12-lead ECG (most important test) to evaluate the cause. It should be done immediately after initial stabilization and taking of vital signs. Most patients with MI will have an abnormal initial ECG: (ST elevation, ST depression, new LBBB, Q waves or T wave inversion) In patients presenting with acute chest pain who have normal ECG, the chance of acute MI is much less than 10%. However, normal ECG doesnot exclude ischemia. An abnormal ECG can also be seen in many non-cardiac conditions (pulmonary embolism, electrolyte abnormalities, aortic dissection) Chest XRAY: It can show other causes of chest pain e.g. pneumothorax, widening of the mediastinum (Aortic dissection), Lung infarction in pulmonary embolism,.. It can also show complications of infarction such as lung congestion from heart failure N.B. Prinzmetal angina, or variant angina: It is a rare condition in which episodes of severe angina is caused by spasm of one of the major coronary arteries. Although the spasm almost always stops spontaneously, Prinzmetal angina may be associated with acute MI, serious ventricular arrhythmias, and sudden death, but in general, the prognosis is good. C/P → Usually occurs during periods of rest, often at night and in the early morning (unlike typical angina), sometimes with history of migraines esp. in women  ECG → ST segment elevation, usually transient during an acute episode of pain (of course at first, you cannot tell who has Prinzmetal variant angina and who has an acute ST elevation MI. Therefore, you must initially treat everyone with chest pain and ST elevation as if they were having an acute MI). Exercise testing and routine coronary angiography usually give normal results. Prinzmetal angina can be confirmed only after coronary angiography Treatment with CCBs or nitrates eliminates spasm in most of these patients. Avoid beta blockers N.B. Nonatherosclerotic ACS : Although thrombotic complications of the atherosclerotic process account for most cases of ACS, a few rare etiologic factors are likely causes of (or contributors to) acute coronary occlusion e.g : o Coronary artery spasm (prinzmetal angina) o Spontaneous coronary dissection (more in young pregnant females) o Coronary artery embolization e.g. atrial myxoma or thrombi o Coronary arteritis o Microvascular angina (previously known as cardiac syndrome X) is the occurrence of angina triggered by coronary microvascular dysfunction due to functional and/ or structural abnormalities in the arterioles and capillaries. These abnormalities reduce the effectiveness of the microvasculature to adapt to myocardial oxygen demands. o Hypercoagulability states such as factor V gene mutation, Deficiencies of proteins C and S, Antithrombin III deficiency and Prothrombin gene mutation o Antiphospholipid antibody syndrome o Anomalous origin of coronary arteries o Cocaine use can induce coronary vasoconstriction in non-diseased coronary segments but is more pronounced in atherosclerotic segments. Unstable Angina AND NSTEMI: (Collectively known as Non-ST Elevation ACS) (NSTE-ACS) UA (unstable angina) is defined as: o Angina of increasing severity/frequency/duration (crescendo angina) o Angina showing increased resistance to nitrates o Angina occurring at rest o New-onset angina UA and NSTEMI are closely related in terms of clinical presentation and pathogenesis. At the time of presentation, UA and NSTEMI may be indistinguishable and can be identically managed. Cardiac markers are used to distinguish NSTEMI from UA. UA is considered as (pre-infarction), thus all patients diagnosed as UA or NSTEMI should be hospitalized for intensive medical treatment. Most patients with NSTE-ACS have a normal physical examination. ECG: An abnormal ECG, particularly dynamic ST-segment deviation or new T-wave inversion will confirm the diagnosis, but the ECG may be normal or show minor changes in up to 50% of cases. 41  Figure showing NSTEMI with ST depression Affecting Leads II, III, and aVF, V5 and V6 High-risk features for patients with UA/NSTEMI: require early angiography Repetitive or prolonged chest pain (>10 min) Prior angioplasty or prior CABG Diabetes Chronic kidney disease Elevated cardiac biomarkers Persistent ECG changes of ST depression > 0.5 mm or new T-wave inversion Hemodynamic instability (SBP 12– 48 hours. Note : If there is contraindication to thrombolysis, then PCI is the only available reperfusion option even if transfer to another facility will take longer than 120 min. 45  Adjuvant therapy used together with reperfusion: (same as NSTEMI) Including dual antiplatelets, parentral anticoagulants, statin, ACE I, beta blockers and nitrates. Discharge medications after ACS include the following: Aspirin, daily for all patients indefinitely Clopidogrel (or Ticagrelor) for up to 12 months after acute myocardial infarction, particularly after stent placement. Beta blockers for all patients after an ACS, continued indefinitely (asthma is not a contraindication for Beta blockers). ACE inhibitors for patients who have CHF with left ventricular dysfunction (ejection fraction 60) More common in obese patients Men > women until after menopause More common in black population at all ages, as is incidence of organ damage Onset usually at the age of 25–55 years Diagnosis: The definition of hypertension differs between international guidelines. Most agree that HTN is diagnosed when systolic BP exceeds 140 or diastolic BP exceed 90 mmHg. 51 White coat Hypertension: As much as 20–25% of mild office hypertension is not actually correct as these patients may have anxiety to the doctor/medical environment (known as “white coat hypertension”). These patients do not have evidence of end-organ damage. Out-of-Office monitoring can help to confirm this diagnosis, using either Home BP monitoring or Ambulatory BP monitoring. Thus, patients, especially with mildly elevated BP, should not be labelled as hypertensive after only a single reading: they can be advised for healthy lifestyle and repeat the readings over several months before confirming the diagnosis and initiating therapy. Classification of Hypertension: The commonly used classification (from European society of Cardiology) is shown in the table below, updated 2024: Category systolic diastolic Non-elevated BP 200 bpm) [with wide QRS complexes] suggest the presence of an accessory pathway (WPW syndrome), with AF. o Co-morbidities: 1.Cardiac conditions: RHD, MV diseases, CAD, CHF, and hypertension. 2.Non-cardiac conditions: hyperthyroidism, hypoxemia, and alcohol intoxication  Classification and Patterns of Atrial Fibrillation o Paroxysmal AF: episode that terminates within 7 days of onset (usually < 24 h) o Persistent: episode lasting > 7 days o Long- standing persistent: episode sustained > 1 year, with decision for a rhythm control strategy o Permanent: AF usually more than a year, with decision to stop additional attempts to restore and maintain normal sinus rhythm. so accepted by the patient and the doctor to become permanent Investigations: ECG: verifies the rhythm as well as identifies other abnormalities such as LVH, pre- excitation, prior MI Chest x-ray: identifies coexisting lung disease Transthoracic Echocardiogram: to detect cardiac co-morbidities e.g. LVH, valvular disease, atrial size Transesophageal echo to rule out left atrial thrombus before cardioversion Thyroid function tests and electrolytes excludes hyperthyroidism/electrolyte abnormalities as a cause of Af Figure showing showing Atrial Fibrillation Treatment: The goals of initial management are: 1. Ventricular rate control 2. Rhythm control (to restore sinus rhythm) 3. Anticoagulation and prevention of embolic complications. 1. Ventricular rate control approach: o Often considered for the patient who has minimal or no symptom. o Target HR is 100 beats/min. ECG → QRS complexes are wide and often bizarre. Causes include cardiomyopathies, infarction, electrolyte disturbances, hypoxia, digitalis toxicity Symptoms include palpitations, concomitant hypotension, CHF, syncope, or cardiac arrest. 103  Signs: (caused by independent and asynchronous atrial and ventricular contractions) o Hypotension or hemodynamic instability. o Intermittent cannon A waves in jugular venous pulses caused by the simultaneous contraction of the atrium and ventricles. Management: o Pulseless VT → treat as VF (cardiac arrest) o VT with pulse and hemodynamically Unstable → DC Synchronized Cardioversion (with sedation) o VT with pulse and hemodynamically Stable → IV Amiodarone or lidocaine then cardioversion if no response 2. TORSADE DE POINTES: A subtype of polymorphic VT is characterized by a gradual change in the amplitude & morphology of QRS complexes with twisting around the isoelectric line. The ventricular rate can range from 150 to 250 bpm. It is associated with a prolonged QT interval, which may be congenital or acquired (medications, electrolyte abnormalities, and ischemia). Treatment: 1. Correct the underlying disorder e.g. replace electrolyte deficits 2. IV magnesium sulfate: can abort the attack in most cases 3. If patient is hemodynamically unstable, give DC cardioversion Figure showing Torsade de Pointes Table showing main drugs causing Long QT and Torsades Remember:Tachyarrhythmias: (check QRS duration → then check regularity) Wide complex (>0.12 s) Narrow complex ( 6 weeks after discontinuation - Accumulation in extracardiac tissues is responsible for the wide spectrum of adverse effects. 113 Mechanism of action: It is a broad-spectrum drug: mainly K+ Channel blocker. In addition, it is a Na+ & Ca++ Channel blocker. It also blocks the beta and alpha adrenoceptors. Extracardiac adverse effect: Although highly safe on the heart, it may cause serious pulmonary and hepatic toxicities. In addition, it can induce wide range of adverse effects e.g. GIT adverse effects, Neurologic adverse effects, Photosensitivity, Goitre with hypo- or hyper-thyroidism Adenosine: Pharmacokinetics: It is rapidly eliminated with ultrashort half-life (15 seconds) → its actions are transient. Cardiac actions, uses and adverse effects: 1) It binds Adenosine A1 receptors →  K+-conductance → Shortens APD & ERP (This Transiently increases vulnerability to AF) 2) 2ry  Ca++-current → delay AVN conduction (It is of choice treatment of reentry types of SVT ) It is given one fast shot and can be repeated in double dose. Non cardiac actions and adverse effects: 1) A1 receptors: Bronchospasm & chest burning → avoid in bronchial asthma 2) A2 receptors: Vasodilatation → Flushing & Headache and even hemodynamic collapse is reported in patients with VT  Cardiosurgery LEARNING OBJECTIVES: Define the different types of cardiac operations Recognize the main surgeries for valvular heart diseases and valve types Recognize complications of mechanical valves and of CABG Types of cardiac operations: Extra-cardiac operations: Carried out on the main vessels or pericardium e.g. pericardiectomy Closed intra-cardiac operations: They include blind procedures performed by instruments or fingers. They used mainly to relieve valve stenosis. They are infrequently used. Open cardiac operations: They are performed under direct vision in a bloodless field in the chambers of the heart or great vessels. To permit this type of surgery the venous inflow to the heart is diverted through an artificial heart lung machine (Extracorporeal circulation). Principles of surgery for acquired valve diseases: 1. Mitral stenosis: o Valvotomy, either closed (does not require cardiopulmonary bypass) or open valvotomy. o Mitral valve replacement, used for calcified valves or double mitral lesions. 2. Mitral incompetence: Mitral valve replacement. 3. Aortic valve diseases: Aortic Valve replacement. *There are several types of prosthetic valves illustrated in figure In general, two kinds of cardiac valve prostheses are used: (1) Bioprosthetic (porcine or bovine) (2) Mechanical (manufactured). Mechanical prostheses have a higher rate of bleeding complications (from anticoagulants), and bioprostheses are more likely to require reintervention (from degeneration). A mechanical valve is usually used in patients who are not planning for pregnancy and in those who have other indications for anticoagulants. These valves require warfarin anticoagulant for life keeping INR around 3. A bioprosthetic valve is recommended to for patients > 65 yr. or expected to have bleeding complications or will not be compliant to anticoagulants. 115  Fig. showing different types of prosthetic valves COMPLICATIONS of prosthetic mechanical valves: 1) Prosthetic valve thrombosis and/or embolism: o Incidence: more with mitral prosthesis o Clinical: Sudden onset of severe breathlessness, pulmonary edema, cardiac arrest. valve sounds are not heard well. o Echo: gradient is increased across the valve; the valve opening is restricted. o Fluoroscopy: the valve mobility is restricted. o Treatment: medical (thrombolysis or heparin) or Surgery 2) Endocarditis (PVE) “see infective endocarditis” 3) Valve dysfunction: o Stenosis: This can happen either due to pannus formation or thrombus obstructing the valve. The gradients are increased and if the patient is symptomatic then immediate treatment is needed, usually re do surgery. o Regurgitation (paravalvular leak): suture dehiscence due to infective endocarditis or technical problem. Some leaks can be closed percutaneously o Mechanical Valve dehiscence: breakdown of sutures leading to detachment of the prosthesis from annulus, causing acute heart failure 4) Hemolysis: o Occurs with para valvular regurgitation, Hemoglobin is low, reticulocytes are increased. Surgery for ischemic heart diseases: “Coronary artery bypass surgery” (CABG) CABG is the preferred treatment for: 1) Disease of the left main coronary artery (LMCA). 2) Disease of all three coronary vessels (LAD, LCX and RCA). 3) Diffuse disease not amenable to treatment with a PCI. Procedure (Simplified): 1) Under general anesthesia and mechanical ventilation, the chest is opened via a median sternotomy (skin incision extends from just below the suprasternal notch to a point several centimeters below the xiphoid process, splitting the sternum). ✓ Advantages: It is associated with less postoperative pain and less interference with pulmonary functions than lateral incisions.  ✓ Disadvantages: Increased risk of wound infection and dehiscence. 2) The bypass grafts are prepared (the internal thoracic arteries, radial arteries or saphenous veins,) and the patient is given heparin to prevent the blood from clotting. 3) The surgeon sutures cannulas into the heart and start cardiopulmonary bypass (CPB). Once CPB is established, the surgeon places the aortic cross-clamp across the aorta and deliver cardioplegia to stop the heart. CPB is also known as Extra- corporeal circulation. 4) One end of each graft is sewn on to the coronary arteries beyond the blockages and the other end is attached to the aorta. 5) The sternum is wired together and the incisions are sutured closed. 6) The patient is moved to the intensive care unit (ICU) to recover. After awakening and stabilizing in the ICU (approximately 1 day), the person is transferred to the cardiac surgery ward until ready to go home (approximately 7 days). Fig. showing heart lung machine Grafts used for bypass: The choice of grafts is highly dependent upon the particular surgeon and institution. 1) The left internal thoracic artery (LITA) (previously referred to as left internal mammary artery or LIMA) 2) The right internal thoracic artery (RITA). 3) The great saphenous vein from the leg. 4) Radial artery from the forearm is frequently used. Graft patency: -Grafts can become diseased and may occlude in months to years after bypass surgery is performed. -Graft patency is dependent on number of factors: 1) The type of graft used (internal thoracic artery, radial artery, or great saphenous vein). 2) The size of the coronary artery that the graft is anastomosed with. Generally: The best patency rates are achieved with the in-situ left internal thoracic artery (the proximal end is left connected to the subclavian artery), Lesser patency rates can be expected with radial artery grafts. Saphenous vein grafts have worse patency rates, but are more available. 117  Figures showing Scar of median sternotomy and types of grafts in CABG Sternal precautions after CABG: 1) Patients need to avoid using their arms excessively, such as pushing themselves out of a chair or reaching back before sitting down. 2) Patients should avoid lifting anything in excess of 5-10 pounds. 3) Finally, patients should avoid overhead activities with their hands, such as reaching for things from the top shelf. Complications of CABG: People undergoing coronary artery bypass are at risk for the same complications as any surgery, plus some risks more common with or unique to CABG. 1. CABG associated complications: o Non-union of the sternum o Myocardial infarction due to embolism, hypoperfusion, or graft failure. o Late graft stenosis, particularly of saphenous vein grafts due to atherosclerosis causing recurrent angina or myocardial infarction. o Acute renal failure due to embolism or hypoperfusion. o Stroke, secondary to embolism or hypoperfusion. 2. General complications: o Deep vein thrombosis (DVT) o Malignant hyperthermia. o Keloid scarring o Wound infection o Wound dehiscence o Chronic pain at incision sites o Chronic stress related illnesses o Death  Revision for OSPE SA nodal arrhythmia: Please revise how to calculate heart rate in case of regular rhythm and irregular rhythm 119 Atrial and AVN arrhythmias: Multifocal Atrial tachycardia Ventricular arrhythmias: Figure showing Torsade de Pointes 121 WPWS: AF + preexcitation Electrical alternans: AV block : RBBB: 123 LBBB: LVH with strain & LAD: RVH with strain & RAD: Anterior STEMI Acute Inferior STEMI: Old inferior MI: 125 Acute Inferior + RV infarction: Acute inferior STEMI + posterior MI (or reciprocal changes): Acute Pericarditis: