Ischemic Heart Disease, Cardiac Arrhythmias Lectures (2024/25) PDF

Lectures in pathophysiology for 5 term Pharmacy Students th Semmelweis University Budapest NET Seminar 6 14th October, 2024. Ischemic heart disease, cardiac arrhythmia Ervi...

Lectures in pathophysiology for 5 term Pharmacy Students th Semmelweis University Budapest NET Seminar 6 14th October, 2024. Ischemic heart disease, cardiac arrhythmia Ervin FINTA MD, PhD Szent Imre Teaching Hospital, VIP-I Department Lectures in pathophysiology for 5 term Pharmacy Students th Semmelweis University Budapest NET Seminar 6 14th October, 2024. Ischemic heart disease, cardiac arrhythmia Ervin FINTA MD, PhD Szent Imre Teaching Hospital, VIP-I Department  ισχαιμία isch-=restriction, hema (haema)=blood Ischemia= restriction in blood supply 2  Ischemia is an absolute or relative shortage of the blood supply to an organ. supply Absolute=limited oxygen supply request Relative=elevated oxygen demand Narrowing of arteries Atherosclerosis Extreme tachycardia Outside compression of blood vessels, e.g. by a tumor Thromboembolism (blood clots) Foreign bodies in the circulation (fat embolism) Limited blood flow Hypotension (septic shock, heart failure) Sickle cell disease (abnormally shaped hemoglobin) Impaired oxygen transporting capacity Anemia, CO poisoning 3  Ischaemia Result: – Oxygen & glucose supply is not enough for the pump function of the heart – Metabolites can not be eliminated from the cells 4  Ischemic heart disease The heart muscle tissue is very sensitive to the ischemia Lack of collateral vessels Oxygen extraction rate is high in rest Phasic blood flow in the coronaries 5  Types of ischemia Subepicardial Subendocardial ischemia ischemia Pressure of blood Pressure of Contracted muscle 6 Mechanism of ischemic heart disease Atherosclerotic plaque formation 7  Ischemic heart disease thrombosis brainmind.com 8 Clinical signs and syptoms of ischemic heart disease Chest pain (angina pectoris) – Burning, squeezing or pressure in the mid- portion of the chest – often accompanied by vegetative signs (e.g. sweating, nausea), and/or left arm, hand, jaw epigastrial pain or discomfort. 9 10  Angina pectoris Retrosternal or precordial reversible chest pain Slideshare.net 11  Angina pectoris Possible causes of the pain in the hypoxic muscle cells – Forced glycolysis-lactate-acidosis – Hypoxia – Spasm of the coronary artery – ??? Connection between hypoxia and pain not fully understood yet 12  Types of angina pectoris Stable Angina – a repeating pattern of chest pain which has not changed in character, frequency, intensity or duration for several weeks Unstable Angina – chest pain that is variable, either increasing in frequency or intensity and with irregular timing or duration Prinzmetal’s or variant angina – caused by vasospasm Microvascular angina – or Syndrome X, occurs when the patient experiences chest pain and positive ECG stress test but has no apparent coronary artery blockage 13  Treatment of angina pectoris AIMS – Relief of syptomps – Slowing progression of the disease – Reduction of the future events like myocardial infarction 14  Treatment of angina pectoris Controlling the risk factors – high blood pressure, diabetes, cigarette smoking (passive as well!!!), high cholesterol levels, excess weight Reduction of myocardial oxygen consumption – Beta blockers, pre- and afterload reduction Augmentation of coronary blood flow – nitrates – Calcium antagonists Improvement of metabolic processes of the myocardium – Trimetazidine Prevention of blood clot formatting – Aspirin, clopidogrel, plasugrel PCI/Surgery (coronary artery bypass) 15  Angina pectoris Decreased Increased coronary Metabolic disturbances oxygen Lactate acidosis… consumption blood flow trimetazidine CAA Increased: Vazospasm Heart rate BB, Verapamil Fixed stenosis PCI, CABG Contractility Thrombus BP lowering drugs Afterload TAI-antiplatelets Nitrate Preload 16  Metabolic modulation (pFOX): Trimetazidine Myocytes Myocardial cells derive their energy via fatty acid and FFA Glucose glucose metabolism. During ischemia the fatty acid pathway predominates. Acyl-CoA Pyruvate However, this pathway requires β-oxidation more oxygen than the glucose Trimetazidine pathway inhibition of fatty acid oxidation Acetyl-CoA should promote a shift towards the more oxygen-efficient glucose pathway. Energy for contraction pFOX = partial fatty acid oxidation FFA = free fatty acid MacInnes A et al. Circ Res. 2003;93:e26-32, Lopaschuk GD et al. Circ Res. 2003;93:e33-7 , Stanley WC. J Cardiovasc Pharmacol Ther. 2004;9(suppl 1):S31-45.  Case presentation – L.S. The patient: L.S Gender: Female Age: 62 Weigh: 86 kg, Height: 167 cm, BMI:30,8 Past medical history: High blood pressure (220/120-150/90 mmHg) Smoking for 40 years, hypercholesterolemia Sometimes feeling of palpitation Known cholelithiasis (a few times cramp) Present Illness: Epigastric and RUQ pain, cramp, after dinner In the Pharmacy asks for spasmolytics The pharmacist can see the patient suffering and sweating after measuring her BP (90/50 mmHg,) calls the What should the pharmacist do? ambulance Actual Treatment: Amlodipin 5 mg b.i.d. 18 Page 18  Emergency Unit P.E. The abdomen was soft, nondistended. Epigastrial and RUQ tenderness. Good bowel sounds present. No hepatosplenomegaly was appreciated. No pulsatile masses were felt. No abdominal bruits were heard. How to continue? 19 Page 19 20 21 22  Myocardial infarction Necrosis of cardiac muscle in the result of interruption of blood supply 23  Symptoms of myocardial infarction Resistant angina- like pain,which is continuous and does not react to nitrates AMI can be silent as well! 24  Complications Congestive heart failure Cardiogenic shock Life-threatening arrhythmia Myocardial rupture Pericarditis Aneurysm 25 Complications Congestive heart failure – Chronic failure of pump function Cardiogenic shock – Usually acute failure of pump function – Heart can not maintain the circulation – Organ perfusion damaged – Prognosis is poor – (needs revascularization and maintenance of circulation eg intra- ortic balloon pump) 26  Complications Myocardial rupture – in the free walls of the ventricles, – the septum between them, – papillary muscles, – or less commonly the atria – 3-5 days after AMI (3 weeks later too) increased pressure against the weakened walls 27  Complications Ventricular aneurysm (local dilation or ballooning of the chamber. Connective tissue!) 28 Complications Life-threatening arrhythmia (Changed electrical characteristics of the infarcted tissue) Re-entry phenomenon – Ventricular tachycardia – Ventricular fibrillation Damaged conduction system – Complete heart block 29  Complications Pericarditis Damage – Inflammation – Pericardium (Heart sac) inflammation 30  Treatment „Time is muscle” Time wasted is muscle lost First line – „MONA”, Morphine, Oxygen, Nitro, Aspirin – Beta blocker, heparin, clopidogrel Second step – Reperfusion- "open artery" principle Percutaneous Coronary intervention PCI Thrombolysis Coronary artery bypass surgery CABG Rehabilitation- QUOL Secondary prevention – Beta blockers, ASA/clopidogrel, ACEi, Statin 31 Short term mortality of acute myocardial infarction 30-day mortality after AMI Hungary vs. Sweden +2-3% Jánosi András , Ofner Péter. Gottsegen György Országos Kardiológiai Intézet. Nemzeti Szívinfarktus Regiszter MKT Balatonfüredi Tudományos Ülése, Balatonfüred 2017. 05. 11-13  Long term mortality after myocardial infarction One-year mortality after AMI Hungary vs. Sweden +8% Jánosi András , Ofner Péter. Gottsegen György Országos Kardiológiai Intézet. Nemzeti Szívinfarktus Regiszter MKT Balatonfüredi Tudományos Ülése, Balatonfüred 2017. 05. 11-13  STEMI –NSTEMI treatment 01.01.2010-09.Nov.2016. Medical treatment at discharge STEMI(%) NSTEMI(%) Aspirin 94,4 92,3 Clopidogrel 90,2 85,3 Prasugrel 4,2 2,38 Béta blokkoló 86,4 87,4 ACE/ARB 85,9 85,9 Statin 90,5 88,6 Ezetimibe 1,4 2,41 https://ir.kardio.hu/ir/fooldal  % 70 Adherence higher than 80% 60 58,7 51,8 50 40 33 30 28,9 20 10 0 clopidogrel statin béta blokkoló aspirin Myocardial infarction registry: only 51,8% of AMI patients purchased at least 80% of the Prescriptions during the 12 month folowing AMI. https://ir.kardio.hu/ir/fooldal  Effect of drug discontinuation (after 1 month) on mortality after Myocardial infarction 36 Arch Intern Med. 2006;166:1842-1847 Percutaneous intervention-stenting 37  38 Prof Merkely Cardiac arrhythmias Cardiac arrhythmias 39  Cardiac arrhythmias Normal electrical activity of the heart 40  Electrical activity of the heart Action potential Threshold potential Resting potential sinus node Resting potential atrial cell Resting potential ventricules 41  Cardiac arrhythmias Arrhythmia = irregular heart rhythm – change in the rhythm (uneven heartbeat) – change in the rate, (very slow or very fast heartbeat) 42  Cardiac arrhythmias Tachycardia(“fast- heart”) Bradycardia (“slow-heart”) Sinus arrhythmia Sinus bradycardia Sinus tachycardia Sick sinus syndrome Premature atrial contractions (PACs) Supraventricular tachycardia (SVT) Paroxysmal atrial tachycardia (PAT Atrial flutter Atrial fibrillation Accessory pathway tachycardias (WPW) AV nodal reentrant tachycardia (AVNRT) Heart block Premature ventricular contractions (PVC's) Ventricular tachycardia (VT) Ventricular fibrillation (VF) 43  Cardiac arrhythmias Premature beat (extrasystole) SUPRAVENTRICULAR 44  Cardiac arrhythmias Premature beat (extrasystole) VENTRICULAR 45 Atrial fibrillation most common abnormal heart rhythm "irregularly irregular" heartbeat with no repeat pattern. about 400 per minute "fire" in the atria – but only a few are transmitted through the AV node. On the ECG, the P wave is replaced by a bumpy line referred to as "fibrillatory waves," and the QRS complex is unevenly and irregularly spaced 46  Complication of the fibrillation- Stroke atria are not contracting effectively – the blood swirls, pools, and may form clots That could travel to the brain brainmind.com 47  Anticoagulation: CHA2DS2-VASc ≥1 CHA2DS2-VASc Score Risk Risk of bleeding: CHF or LVEF < 1 HAS-BLED score ≥ 3 40% Hypertension 1 Age > 75 2 Diabetes 1 Stroke/TIA/ 2 Thromboembolism Vascular 1 Disease Age 65 - 74 1 Female 1 From ESC AF Guidelines 48 http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-afib-FT.pdf  Anticoagulation is recommended: CHA2DS2-VASc score ≥ 1 Risk of bleeding: caution and regular review of the patient is needed: HAS-BLED score ≥ 3 49 Atrial fibrillation-atrial flutter Fibrillation 50 Cardiac arrhythmias 51  Cardiac arrhythmias Atrial fibrillation 52  Reentry mechanism Normal tissue Purkije fiber forms two branches APs travel down each APs cancel each other out 53  Reentry mechanism Unidirectional block (retrograde conduction only) APs travel down on branch2 into the common distal path Travel retrograde through the unidirectional block if it finds the tissue excitable AP will continue by traveling down 54  Reentry mechanism Necessary conditions for the reentry Unidirectional block within a conducting pathway Critical timing Length of the effective refractory period 55  Global reentry PSVT Necessary conditions for the reentry Unidirectional block within a conducting pathway Critical timing Length of the effective refractory period Accessory pathway WPW 56 Cardiac arrhythmias 57 58  Conduction abnormalities Blocks – Sino-atrial – Atrio-ventricular 1st degree (PR interval prolonged) 2nd degree – Type I (Mobitz I) – Type II (Mobitz II) 3rd degree (complete heart block) – Intraventricular – Bundle branch blocks » Left bundle branch block (LBBB) » Right bundle branch block (RBBB) – Fascicular blocks » Left anterior fascicular block » Left posterior fascicular block » Right fascicular block Conductionsystemofthe heart.png 59 Sino-atrial block www.unm.edu 60  First-degree atrio-ventricular block prolonged PR interval of >200 milliseconds (5 small squares) www.onlinelege.no 61  Second-degree atrio-ventricular block Type I (Mobitz I or Wenckebach AV block) Repeated pattern of progressive prolongation of the PR interval, which results in the failure of conduction of one atrial beat 62 www.ecg.edu  Second-degree atrio-ventricular block Type II (Mobitz II) Constant PR interval, but occasionally atrial depolarization is not followed by ventricular depolarization www.ecg.edu 63  Third-degree atrio-ventricular block Complete heart block Complete dissociation of the P waves and QRS complexes www.acls.com 64  Intraventricular conduction disturbances examples 65  ECG leads RIGHT LEFT INFERIOR WALL www.medicaltechblog.com 66 Left bundle block QRS duration of > 120 ms Dominant S wave in V1 Broad monophasic R wave in lateral leads (I, aVL, V5-V6) Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL) Prolonged R wave peak time > 60ms in left precordial leads (V5-6) 67  Left bundle block QRS duration of > 120 ms Dominant S wave in V1 Broad monophasic R wave in lateral leads (I, aVL, V5-V6) Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL) Prolonged R wave peak time > 60ms in left precordial leads (V5-6) www.proprofs.com 68 Right bundle block Broad QRS > 120 ms RSR’ pattern in V1-3 (‘M- shaped’ QRS complex) Wide, slurred S wave in the lateral leads (I, aVL, V5-6) 69  Right bundle block Broad QRS > 120 ms RSR’ pattern in V1-3 (‘M-shaped’ QRS complex) Wide, slurred S wave in the lateral leads (I, aVL, V5-6) http://hqmeded-ecg.blogspot.hu/ 70  Cardiac arrhythmias- Treatment Drug treatments – antiarrhythmic drugs to convert the arrhythmia to a normal sinus rhythm or to prevent an arrhythmia. – Other medications heart-rate control drugs; anticoagulants; antiplatelet drugs Lifestyle changes – Avoiding of Alcohol, Caffeine, Stimulants Cardioversion – Electrical, chemical Pacemaker implantation Catheter ablation therapy Implantable cardioverter-defibrillator 71  Electrical cardioversion Medicinenet.com 72 When to advise to seek medical care? Chest pain: always Irrregular heart beat feeling: always 73 When to call an ambulance? Resistant chest pain Chest pain or palpitation feeling with vegetative signs 74 Thank you for the attention! Ervin FINTA Szent Imre Teaching Hospital Budapest VIP-I Department 75