{"id":8288,"date":"2012-05-01T05:15:50","date_gmt":"2012-05-01T05:15:50","guid":{"rendered":"http:\/\/www.homeobook.com\/?p=8288"},"modified":"2022-01-06T01:06:34","modified_gmt":"2022-01-06T01:06:34","slug":"ischemic-heart-disease-and-homoeopathy","status":"publish","type":"post","link":"https:\/\/www.homeobook.com\/ischemic-heart-disease-and-homoeopathy\/","title":{"rendered":"Ischemic Heart Disease and Homoeopathy"},"content":{"rendered":"
Dr Beenadas<\/strong><\/p>\n Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium; it typically occurs when there is an imbalance between myocardial oxygen supply and demand.<\/p>\n Epidemiology Risk factors Many of these risk factors are modifiable. Non-modifiable risk factors include age, sex, and family history – genetic predisposition.<\/p>\n Pathophysiology Pathophysiology of MI includes concept of myocardial supply<\/strong> and demand.<\/strong><\/p>\n By reducing the lumen of the coronary arteries –\u00a0\u00a0 by spasm, atherosclerosis, aortitis, arterial thrombi, aortic stenosis –\u00a0 limits appropriate increases in perfusion when the demand for flow is augmented, as occurs during exertion or excitement.<\/p>\n The major determinants of myocardial oxygen demand (MVO2<\/sub>) are heart rate, myocardial contractility, and myocardial wall tension (stress).<\/p>\n Not infrequently, two or more causes of ischemia\u00a0 can coexist.<\/p>\n Pathology of Coronary Atherosclerosis If\u00a0 the diameter of an epicardial artery\u00a0 reduces by 50%, there is a limitation on the ability to increase flow to meet increased myocardial demand. When\u00a0\u00a0 reduced by ~80%, blood flow at rest may be reduced, and further minor decreases\u00a0 can reduce coronary flow dramatically and cause myocardial ischemia.<\/p>\n The pathogenesis can include: Vasospasm – with or without coronary atherosclerosis and possible association with platelet aggregation.<\/p>\n Emboli – from left sided mural thrombosis, vegetative endocarditis, or paradoxic emboli from the right side of heart through a patent foramen ovale.<\/p>\n The gross morphologic appearance<\/strong> include: Subendocardial infarct – multifocal areas of necrosis confined to the inner 1\/3-1\/2 of the left ventricular wall.<\/p>\n Cardiovascular Disease Classification <\/strong><\/p>\n <\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n By zone Patterns of Ischemic Heart Disease (IHD) 1. Stable angina (typical) – paroxysms of pain related to exertion and relieved by rest or vasodilators. subendocardial ischemia with ST-segment depression<\/p>\n 2.Variant or Prinzmetal’s angina – angina that classically occurs at rest and is caused by reversible spasm in normal to severely atherosclerotic coronary arteries. ST-segment elevation or depression maybe seen during attacks.<\/p>\n 3.Unstable angina – prolonged pain, pain at rest in a person with stable angina, or worsening of pain in stable angina. ST-segment depression (usually) and ST-segment elevation.<\/p>\n 4.Sudden cardiac death – Unexpected death from cardiac causes usually within one hour after a cardiac event or without the onset of symptoms. Usually high-grade stenosis with acute coronary change<\/p>\n Symptoms Diagnosis 2. Cardiac markers \u2013 blood tests for heart muscle cell damage. The most often used markers are the creatine kinase-MB (CK-MB), it rises in serum within 2 to 8 hours of MI\u00a0 and the troponin I (TnI) or troponin T (TnT) levels. Troponins will remain elevated longer than CK–up to 5 to 9 days for troponin I and up to 2 weeks for troponin T. Troponin T lacks some specificity because elevations can appear with skeletal myopathies and with renal failure.<\/p>\n Myoglobin:<\/strong> can help to determine the size of an infarction, but not specific for cardiac muscle, and can be elevated with any form of injury to skeletal muscle.<\/p>\n Lactate dehydrogenase:<\/strong> rise in 12 to 24 hours following MI, and peaks in 2 to 3 days, Measurement of LDH isoenzymes is greater specificity for cardiac injury. There are 5 isoenzymes (1 through 5). Ordinarily, isoenzyme 2 is greater than 1.<\/p>\n 3.\u00a0 coronary angiogram – visualization of narrowings or obstructions on the heart vessels\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 4.\u00a0 chest X-ray<\/p>\n Diagnostic criteria\u00a0–\u00a0\u00a0<\/strong>WHO criteria\u00a0 – the diagnosis of myocardial infarction requires two out of three components<\/p>\n Physical examination If heart failure ensues, elevated JVP and hepato lugular reflex, or swelling of the legs.\u00a0 Third and fourth HS,\u00a0\u00a0 systolic murmers, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung.<\/p>\n Treatment Complications<\/strong><\/p>\n HOMOEOPATHIC APPROACH Sycosis\u00a0\u00a0 <\/strong>From suppression of rheumatic complaints \u2013 RHD,AR\/MR, hypertrophy of heart and valvular disorders. Pains in eletric shocks, radiates\u00a0 from precordium to the shoulder scapula.soreness or tenderness over precordium. Heat and change of waether<; > from gentle exercise, exept of rheumatic origin. Pulse is slow, feeble and soft. Cardiac dropsy, tachycardia, thrombosis, embolism, MI are sycotic manifestations.<\/p>\n Syphilis\u00a0–\u00a0 <\/strong>Heart affections with valvular degeneration. Sensation of heaviness in precordium. Symptoms are < at night, perspiration, warmth of bed. > during day, change of possition and cold. .Pulse irregular in rate or rythem.<\/p>\n Homoeopathic\u00a0\u00a0 Management KENTS\u00a0 REPERTORY –\u00a0 <\/strong>Chest \u2013 Angina pectoris 3 marks \u2013 am.carb, apis,arg.nit, arn, ars, aur, aur.m, cact, lat.mac, naja, ox.ac, phos, rhus.tox, spigi, spongi,<\/p>\n 2 marks – acon, amyl, chel. Chin.sulph, cimici, cup.ars, digi, dios, hep.s, jug.c, kali.ca, kalmia, lache, lauro, lyco, mag.phos, mosch, nux.v, sambu, stramo, tab, tarentu, ther, verat.<\/p>\n Dr Beenadas Dr Beenadas Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium; it typically occurs when there is an imbalance between […]<\/a><\/p>\n<\/div>","protected":false},"author":1,"featured_media":43021,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[115],"tags":[1960],"class_list":{"0":"post-8288","1":"post","2":"type-post","3":"status-publish","4":"format-standard","5":"has-post-thumbnail","7":"category-practice-of-medicine","8":"tag-ischemic-heart-disease-and-homoeopathy"},"yoast_head":"\n
\n<\/strong>Myocardial infarction is a common presentation of IHD.\u00a0 In India, cardiovascular disease (CVD) is the leading cause of death. CVD\u00a0 affects Indians at a younger age, in their 30s and 40s. IHD is likely to become the most common cause of death worldwide by 2020.<\/p>\n
\n<\/strong>Risk factors for\u00a0 atherosclerosis are generally risk factors for myocardial infarction. They are diabetes mellitus, hyperlipidemia, hypertension, cigarette smoking, family history of premature IHD,\u00a0 advanced age, male gender, the postmenopausal state, obesity,\u00a0 high stress, OCP, inflammation- Elevated CRP blood levels, can predict the risk of MI, stroke and development of diabetes.<\/p>\n
\n<\/strong>Under normal conditions, for any given level of a demand for oxygen, the myocardium will be supplied with oxygen-rich blood to prevent underperfusion of myocytes and the subsequent development of ischemia and infarction.<\/p>\n
\n<\/strong>Epicardial coronary arteries are the major site of atherosclerotic disease. The risk factors\u00a0 leads to inappropriate constriction, luminal thrombus formation, and abnormal interactions with blood leukocytes, especially monocytes, and platelets. Monocyte interaction ultimately results in the subintimal collections of fat, smooth-muscle cells, fibroblasts, and intercellular matrix – atherosclerotic plaques, which develop at irregular rates\u00a0 of the epicardial coronary tree.<\/p>\n
\n<\/strong>Occlusive intracoronary thrombus – a thrombus overlying an ulcerated or fissured stenotic plaque causes 90% of transmural acute myocardial infarctions.<\/p>\n
\n<\/strong>Transmural infarct – involving the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%. Isolated infarcts of RV and right atrium are extremely rare.<\/p>\n\n\n
\n \n \n\n
\n Class<\/strong><\/td>\n New York Heart Association Functional Classification<\/strong><\/td>\n Canadian Cardiovascular Society Functional Classification<\/strong><\/td>\n<\/tr>\n<\/thead>\n\n \n I<\/strong><\/td>\n Patients have cardiac disease but without<\/em> the resulting limitations<\/em> of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.<\/td>\n Ordinary physical activity, such as walking and climbing stairs, does not cause angina<\/em>. Angina present with strenuous or rapid or prolonged exertion at work or recreation.<\/td>\n<\/tr>\n \n II<\/strong><\/td>\n Patients have cardiac disease resulting in slight limitation<\/em> of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.<\/td>\n Slight limitation<\/em> of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, or when under emotional stress or only during the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of stairs at a normal pace and in normal conditions.<\/td>\n<\/tr>\n \n III<\/strong><\/td>\n Patients have cardiac disease resulting in marked limitation<\/em> of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain.<\/td>\n Marked limitation<\/em> of ordinary physical activity. Walking one to two blocks on the level and climbing more than one flight of stairs in normal conditions.<\/td>\n<\/tr>\n \n IV<\/strong><\/td>\n Patients have cardiac disease resulting in inability<\/em> to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.<\/td>\n Inability<\/em> to carry on any physical activity without discomfort\u2014anginal syndrome may be present at rest.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<\/div>\n
\n<\/strong>Depending on the location of the obstruction, different zones of the heart can become injured –\u00a0 anterior, inferior, lateral, apical, septal, posterior, and right-ventricular infarctions (and combinations).<\/p>\n\n
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\n<\/strong>Angina pectoris – a symptom complex of IHD characterized by paroxysmal attacks of chest pain, usually substernal or precordial, caused by myocardial ischemia that falls short of inducing infarction. There are several patterns:<\/p>\n
\n<\/strong>Chest pain –\u00a0 is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Pain radiates most often to the left arm, but may also radiate to the lower\u00a0 jaw, neck, right arm,\u00a0 back and epigastrium,. Levine’s sign, in which the patient localizes the chest pain by clenching their fist over the sternum,<\/p>\n\n
\n<\/strong>1. ECG –\u00a0 ST elevation MI<\/strong> (STEMI) or non-ST elevation MI<\/strong> (NSTEMI). Most cases of STEMI are treated with\u00a0 thrombolysis or if possible with\u00a0 percutaneous coronary intervention (PCI, angioplasty and stent insertion). NSTEMI is managed with medication, although PCI is often performed during hospital admission.<\/p>\n\n
\n<\/strong>Increased\u00a0 RR, cool and\u00a0 pale skin due to vasoconstriction,\u00a0 low-grade fever (38\u201339 \u00b0C).\u00a0 BP be elevated or decreased, and the\u00a0 pulse can be become\u00a0 irregular.<\/p>\n
\n<\/strong>Pain relief drug, reperfusion of complete occlusion of a coronary artery, t<\/strong>hrombolytic therapy, Primary percutaneous coronary intervention.<\/p>\n\n
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\n<\/strong>Psora-\u00a0\u00a0<\/strong>Many psoric heart troubles are functional. And accompanied with much anxiety, mental distress and fear of incurable disease or death. Feeling of increased circulatory function \u2013 congession and plethora. Sharp, cutting, neuralgic pains about the heart.\u00a0 Pains are < in the evening, from movement, coughing, laughing and eating. Symptoms are > from eructations, rest and lying down. Sensation of band around heart. Pulsations shake the whole body. Bradycardia.<\/p>\n
\n<\/strong>BOERICK\u2019S – <\/strong>\u00a0Circulatory system \u2013 Pain \u2013 Angina pectoris2 marks \u2013 acon, amyl,ars, cact, cimi, cocaine, crat,\u00a0 cuprum. Ac, glono, hematox,hydroc.ac, latro, mag.phos, naja, nat.iod, nux.vom, ox.ac, spig, spong, tab,<\/p>\n\n
\n<\/strong>Lecturer, Department of MM
\nGovt. Homeopathic Medical College. Calicut<\/p>\n","protected":false},"excerpt":{"rendered":"