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.
Myocardial infarction is a common presentation of IHD. In India, cardiovascular disease (CVD) is the leading cause of death. CVD 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.
Risk factors for atherosclerosis are generally risk factors for myocardial infarction. They are diabetes mellitus, hyperlipidemia, hypertension, cigarette smoking, family history of premature IHD, advanced age, male gender, the postmenopausal state, obesity, high stress, OCP, inflammation- Elevated CRP blood levels, can predict the risk of MI, stroke and development of diabetes.
Many of these risk factors are modifiable. Non-modifiable risk factors include age, sex, and family history – genetic predisposition.
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.
Pathophysiology of MI includes concept of myocardial supply and demand.
By reducing the lumen of the coronary arteries – by spasm, atherosclerosis, aortitis, arterial thrombi, aortic stenosis – limits appropriate increases in perfusion when the demand for flow is augmented, as occurs during exertion or excitement.
The major determinants of myocardial oxygen demand (MVO2) are heart rate, myocardial contractility, and myocardial wall tension (stress).
Not infrequently, two or more causes of ischemia can coexist.
Pathology of Coronary Atherosclerosis
Epicardial coronary arteries are the major site of atherosclerotic disease. The risk factors 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 of the epicardial coronary tree.
If the diameter of an epicardial artery reduces by 50%, there is a limitation on the ability to increase flow to meet increased myocardial demand. When reduced by ~80%, blood flow at rest may be reduced, and further minor decreases can reduce coronary flow dramatically and cause myocardial ischemia.
The pathogenesis can include:
Occlusive intracoronary thrombus – a thrombus overlying an ulcerated or fissured stenotic plaque causes 90% of transmural acute myocardial infarctions.
Vasospasm – with or without coronary atherosclerosis and possible association with platelet aggregation.
Emboli – from left sided mural thrombosis, vegetative endocarditis, or paradoxic emboli from the right side of heart through a patent foramen ovale.
The gross morphologic appearance include:
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.
Subendocardial infarct – multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall.
Cardiovascular Disease Classification
Depending on the location of the obstruction, different zones of the heart can become injured – anterior, inferior, lateral, apical, septal, posterior, and right-ventricular infarctions (and combinations).
- For example, an occlusion of the LAD artery will result in an anterior wall myocardial infarct.
- Infarcts of the lateral wall are caused by occlusion of Left Circumflex artery or its oblique marginal branches (or even large diagonal branches from the LAD.)
- Both inferior wall and posterior wall infarctions may be caused by occlusion of either the RCA or the left circumflex artery, depending on which feeds the posterior descending artery
- Right ventricular wall infarcts are also caused by RCA occlusion.
Patterns of Ischemic Heart Disease (IHD)
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:
1. Stable angina (typical) – paroxysms of pain related to exertion and relieved by rest or vasodilators. subendocardial ischemia with ST-segment depression
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.
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.
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
Chest pain – 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 jaw, neck, right arm, back and epigastrium,. Levine’s sign, in which the patient localizes the chest pain by clenching their fist over the sternum,
- Shortness of breath – occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure
- Other symptoms – diaphoresis, weakness, light-headedness, nausea, vomiting and palpitations.
- MI in women include dyspnoea, weakness, and fatigue. Fatigue, Chest pain may be less predictive of coronary ischemia.
- Approximately one fourth of all myocardial infarctions are silent – in the elderly, in DM and after heart transplantation,
1. ECG – ST elevation MI (STEMI) or non-ST elevation MI (NSTEMI). Most cases of STEMI are treated with thrombolysis or if possible with percutaneous coronary intervention (PCI, angioplasty and stent insertion). NSTEMI is managed with medication, although PCI is often performed during hospital admission.
2. Cardiac markers – 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 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.
Myoglobin: 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.
Lactate dehydrogenase: 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.
3. coronary angiogram – visualization of narrowings or obstructions on the heart vessels 4. chest X-ray
Diagnostic criteria – WHO criteria – the diagnosis of myocardial infarction requires two out of three components
- Clinical history of ischaemic type chest pain lasting for more than 20 minutes
- Changes in serial ECG tracings – pathological Q waves, ST elevation or depression
- Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin
Increased RR, cool and pale skin due to vasoconstriction, low-grade fever (38–39 °C). BP be elevated or decreased, and the pulse can be become irregular.
If heart failure ensues, elevated JVP and hepato lugular reflex, or swelling of the legs. Third and fourth HS, systolic murmers, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung.
Pain relief drug, reperfusion of complete occlusion of a coronary artery, thrombolytic therapy, Primary percutaneous coronary intervention.
- Immediate- is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.
- chronic –
- Congestive heart failure
- Myocardial rupture
- Life-threatening arrhythmia
- Pericarditis – As a reaction to the damage of the heart muscle, inflammatory cells are attracted. The inflammation may reach out and affect the heart sac, called pericarditis. In Dressler’s syndrome, this occurs several weeks after the initial event.
- Cardiogenic shock
Psora- 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 – congession and plethora. Sharp, cutting, neuralgic pains about the heart. 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.
Sycosis From suppression of rheumatic complaints – RHD,AR/MR, hypertrophy of heart and valvular disorders. Pains in eletric shocks, radiates 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.
Syphilis – 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.
BOERICK’S – Circulatory system – Pain – Angina pectoris2 marks – acon, amyl,ars, cact, cimi, cocaine, crat, cuprum. Ac, glono, hematox,hydroc.ac, latro, mag.phos, naja, nat.iod, nux.vom, ox.ac, spig, spong, tab,
KENTS REPERTORY – Chest – Angina pectoris 3 marks – am.carb, apis,arg.nit, arn, ars, aur, aur.m, cact, lat.mac, naja, ox.ac, phos, rhus.tox, spigi, spongi,
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.
- CACTUS GRANDIFLORIS :– Constriction; whole body feels as if caged, with wire being twisted tighter and tighter. Heart feels as if clasped and unclapsed rapidly by an iron hand. very acute pains and stitches in heart; pulse feeble,irregular, quick, without strength. Heart weakness of arterio-sclerosis. Violent palpitation; worse lying on left side.
- CRATAEGUS:– Said to have a solvent power upon crustaceous and calcareous deposits in arteries. For artherosclerosis and cardiac dropsy. Extreme dyspnoea on least exertion. Pulse irregular, feeble, intermittent.
- LATRODECTUS MACTANS.- Violent, praecordial pain extending to the axilla and down the arm and forearm to fingers, with numbness of the extremity. Pulse feeble and rapid.
- CIMICIFUGA RACEMOSA – Angina pectoris. Irregular, slow, trembling pulse. Numbness of left arm; feels as if bound to side. Heart’s action ceases suddenly, impending suffocation.
- LAUROCERASUS.- Clutching at heart and palpitation. Mitral regurgitation.
- HYDROCYANIC ACID.:- Violent palpitation. Pulse, weak irregular. Torturing pain in chest. Cold extremities. Angina pectoris. [Spigel.; Oxal. ac.]
- CUPRUM METALLICUM – Angina pectoris. Slow pulse; or hard, full and quick. Palpitation, praecordial anxiety and pain. Fatty degeneration. [Phytol.]
- LACHESIS- Constricted feeling causing palpitation, with anxiety. Palpitation, with fainting spells, especially during climacteric. Irregular beats.
- CROTALUS HORRIDUS – Heart’s action ceases suddenly, impending suffocation.Trembling feeling of heart. Action feeble, pulse tremulous.
- KALMIA LATIFOLIA – Palpitation; worse leaning forward. Weak, slow pulse. [Dig.; Apoc. can.] Fluttering of heart, with anxiety. Sharp pains take away the breath. Shooting through chest above heart into shoulder-blades.
- HAEMATOXYLON – Sense of constriction is characteristic. Sensation as if a bar lay across chest. Angina pectoris. Convulsive pain in heart region with oppression.
- KALI CARBONICUM – Palpitation and burning in heart region. Sensation as if heart were suspended. Weak, rapid pulse; intermits, due to digestive disturbance. Threatened heart failure.
- JUGLANS CINEREA – Pain in chest, axilla and scapula, with suffocative sensation. Feeling as if all internal organs were too large, especially those of left side.
- IODUM – Heart feels squeezed, as if by an iron hand [Cactus] followed by great weakness and faintness. Palpitation from least exertion. Tachycardia. Myocarditis, painful compression around heart.
- GLONOINE – Palpitation with dyspnoea. Any exertion brings on rush of blood to heart and fainting spells.
- OXALICUM ACIDUM – Heart symptoms alternate with aphonia, angina pectoris; sharp, lancinating pain in left lung coming on suddenly, depriving of breath. Praecordial pains which dart to the left shoulder. Palpitation and dyspnoea in organic heart disease; worse, when thinking of it.
- FERRUM METALLICUM – Palpitation; worse, movement. Pulse full, but soft and yielding; also, small and weak. Heart suddenly bleeds into the blood vessels, and as suddenly draws a reflux, leaving pallor of surface.
- DIGITALIS – the pulse is weak, irregular, intermittent, abnormally slow. Great weakness and sinking of strength, faintness, coldness of skin, and irregular respiration; Stimulates the heart’s muscle. Pulse weak, and quickened by least movement. The least movement causes violent palpitation, and sensation as if it would cease beating, if he moves. [Opposite; Gels.]
- BUFO – Heels too large. Constriction about heart. Sensation of heart swimming in water. Palpitation.
- NAJA TRIPUDIANS – Its action settles around the heart; valvular troubles. Hypertrophy, and valvular lesions. Angina pains extending to nape of neck, left shoulder and arm with anxiety and fear of death. Pulse irregular in force. Acute and chronic endocarditis. Palpitation.
- AMYL NITROSUM – Praecordial anxiety. Pain and constriction around heart. Fluttering at slightest excitement. Palpitation of the heart and especially the flushing and other discomforts at climacteric. On inhaling this drug, it rapidly dilates all arterioles and capillaries, producing flushing
- MAGNESIA PHOSPHORICA – Angina pectoris. Nervous spasmodic palpitation. Constricting pains around heart.
- AMMONIUM CARB – Audible palpitation with fear, cold sweat, lachrymation, inability to speak, loud breathing and trembling hands. Heart weak, wakes w ws ’95.ith difficult breathing and palpitation.
- SPIGELIA – Praecordial pain and great aggravation from movement. Pulse weak and irregular. Angina pectoris. Neuralgia extending to arm or both arms. Craving for hot water which relieves. Dyspnoea; must lie on right side with head high.
- ADONIS VERNALIS. – muscles of the heart are in stage of fatty degeneration, regulate the pulse and increase the power of contractions of heart. Low vitality, with weak heart and slow, weak pulse. Mitral and aortic regurgitation. Myocarditis, irregular cardiac action, constriction and vertigo. Praecordial pain, palpitation, and dyspnoea.
- SPONGIA TOSTA – Angina pectoris; faintness, and anxious sweat. Awakened suddenly after midnight with pain and suffocation; is flushed, hot, and frightened to death. [Acon.] Rapid and violent palpitation, with dyspnoea; cannot lie down.
- ACONITUM NAPELLUS :- Affections of the heart with pain in left shoulder. Palpitation, with anxiety, fainting, and tingling in fingers. Pulse full, hard; tense and bounding; sometimes intermits.
- TABACUM – Should prove the most homoeopathic drug for angina pectoris, with coronaritis and high tension (Cartier). Angina pectoris, pain in praecordial region. Palpitation when lying on left side. pain in praecordial region. Pain radiates from center of sternum. Acute dilatation caused by shock or violent physical exertion (Royal). Tachycardia. Bradycardia.
- VERATRUM ALBUM – Palpitation with anxiety and rapid audible pertrrespiration. Pulse irregular, feeble. Tobacco heart from chewing.
- STROPHANTHUS HISPIDUS – Hearts action weak, rapid, irregular, due to muscular debility and insufficiency.
- IBERIS – Pulse full, regular, intermittent. Violent palpitation induced by slighest exertion, laughing or coughing. Cardiac dyspnoea.
- TARENTULA HISPANIA – Palpitation; praecordial anguish, sensation as if heart twisted and turned around.
Lecturer, Department of MM
Govt. Homeopathic Medical College. Calicut
Modern life exertion,olden era homeopaths call it muscular contraction excess this contracts veins and excess blood quantity flow to heart if not accomodated by minor heart muscle dilation lead to angina pain so ELASTICITY factor of heart muscle major reason for most of off on angina pains second factor coronary arteries defect,they also say tricuspid valve reflux action push back some blood to auricle and great veins acts as SAFETY valve to control volume pumped by left heart.mitral black flow they say also helps breathing.allopaths do not improve elasticity but control blood flow rate by blocking certain chemical paths.govt agencies should videly publicise go first to a homeopath unless disease is of pathological changes nature.
Edwin Hale expert homeopath on heart,Endocarditis mostly caused by rheumatic complications is sub acute inflammation and inflammation morbid products namely lymph exudation extra fibrin in blood cause vegetation granular mass heart area simple language of homeopaths a polypi of heart,cause malfunction even of valves visible as excited palpitating hypertrophic heart plus these morbid products if block capillary circulation this causes secondary inflammation in organs esp kidney.remedy asclepias for endocarditis with renal affections and baptisia low state typhod like fevers is recommended both in q or 1x.cactus 1x if severe palpitation and band like constriction,cimicifuga nervous female to ease heart muscle contraction.this doctor says endocarditis is silent killer because signs are vague whereas pericardtis serous membrane inflammation calls for immediate attention lachesis type.naja 30 is overall heart tonic for chronic endocarditis.arnica keeps circulation intact and helps blood flow to washout morbid products.non professionals with interest in homeopathy keep them fit by occasional dose of rhus tox 200 and arnica 30 and heart muscle stimulator mixtures like tonicard sbl washout kidney by drox23 haslab.
being non professional with interest in homeopathy i try to find what old era homeopaths advise,angina pectoris best article is by Leo Bonnin.he says females nervous anxiety angina best is cimicifuga,cactus for chest constriction,argt nit if pain felt after eating.he says best for pseudo angina is latrodectus mac 6c.of course in emergency blood vessel dilation to allow blood flow to heart muscle is imp he says glonoin low potency works but allopaths nitrate tablet for instant action need not be ignored.
What a bogus article it is . Hi is there any necessity of publishing this article where as any interested person go through Therpeutics and find out this list of drugs.
What is needed u must share your own experience in this field. Do u understand friend?
The article is valuable to a homoeopathic physician only, not to a commoner who wants to cure his heart disease by studing online materials. It has to be understood that Dr. Beenadas has only provided some leading symptoms of a few medicines useful in cardiac diseases. He has not prescribed them.
what you give to patient,you give all the medicine or what,sir this not right,it is copy down business,i saw your article with a faith so we can manage IHD,but you just do donkey work,not scientific work,why you upload this article,is it research done by you? no then why you excited us or give faith we can manage these medical emergencies.