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HEART SPECIALISTS IN YELAHANKA NEW TOWN BANGALORE Mitral stenosis Rheumatic mitral stenosis is rare in developed countries but is an important cause of maternal and fetal morbidity and mortality in many parts of the world. Mitral stenosis is often poorly tolerated because of the shortened diastolic filling period that occurs during pregnancy. A mitral valve area of less than 1.5 cm2) means a considerable risk to the mother of pulmonary oedema as pregnancy proceeds. Even previously asymptomatic patients are at risk. Close follow-up and regular echocardiograms are indicated. Treatment to slow the heart and increase the length of diastole (beta-blockers) should be commenced if symptoms (dyspnoea) appear or the Doppler echo measurement of pulmonary artery pressure exceeds 50 mmHg Diuretics may improve symptoms but for severe stenosis balloon valvotomy can be performed during pregnancy.30 There are risks to the mother and fetus associated with the procedure, which should be performed only at an experienced centre and only for severe stenosis. Aortic stenosis Delivery is usually well tolerated by women with aortic stenosis unless they are very symptomatic. If heart failure has developed, balloon valvotomy of the valve is safer than surgical replacement. The procedure provides temporary relief of symptoms. Mechanical prosthetic valves and pregnancy
THE BEST HEART SPECIALISTS IN BANGALORE Angioplasty Balloon dilatation of coronary artery stenoses was first performed in the late 1970s by Andreas Grunzig. The technique has undergone many refinements and is now widely used for the treatment of angina not responding to medical treatment. Angioplasty has not been shown to improve the prognosis of patients with stable angina. Coronary artery bypass grafting (CABG) has similarly not been shown to prolong life for most stable angina patients. However, both treatments are very successful in relieving the symptoms of angina. The COURAGE Trial compared optimal medical treatment of angina with angioplasty but excluded patients with symptoms refractory to medical treatment.1 Not surprisingly, this group of stable mild angina patients had a similar outcome with angioplasty and medical treatment. The trial suggests that compared with optimal medical treatment, angioplasty is a safe and slightly more effective treatment for stable angina. Patients can make an informed choice between these two treatments. The majority of patients treated with angioplasty in Australia have acute coronary syndromes and here there is good evidence of prognostic benefit with angioplasty compared with medical treatment. In many centres one-, two- and complicated three-vessel disease are managed this way. It has been shown to be as effective as coronary surgery for these patients but at the price of a higher rate of re-intervention. This is because the greatest limitation of angioplasty is the rate of restenosis in vessels that have been dilated. Restenosis
DIABETIC SPECIALIST IN YALAHANKA Syncope and dizziness The history Syncope is a transient loss of consciousness resulting from cerebral anoxia, usually due to inadequate blood flow. Syncope may represent a simple faint or be a symptom of cardiac or neurological disease. Establish whether the patient actually loses consciousness and under what circumstances the syncope occurs—for example, on standing for prolonged periods or standing up suddenly (postural syncope), while passing urine (micturition syncope), on coughing (tussive syncope) or with sudden emotional stress (vasovagal syncope). Find out whether there is any warning such as dizziness or palpitations, and how long the episodes last. Recovery may be spontaneous or require attention from bystanders. Bystanders may also have noticed abnormal movements if the patient has epilepsy, but these can also occur in primary syncope. If the patient’s symptoms appear to be postural, enquire about the use of anti-hypertensive or anti-anginal drugs and other medications that may induce postural hypotension. If the episode is vasovagal, it may be precipitated by something unpleasant like the sight of blood, or it may occur in a hot crowded room; patients often feel nauseated and sweaty before fainting and may have had prior similar episodes, especially during adolescence and young adulthood. The diagnosis of this relatively benign and very common cause of syncope can usually be made from the history. Patients with very typical symptoms rarely require extensive investigations. If syncope is due to an arrhythmia there is often sudden loss of consciousness regardless of the patient’s posture. A history of rapid and irregular palpitations or a diagnosis of atrial fibrillation in the past suggests the possibility of sick sinus syndrome. These patients have intermittent tachycardia, usually due to atrial fibrillation, and episodes of profound bradycardia, often due to complete heart block. Chest pain may also occur if the patient has aortic stenosis or hypertrophic cardiomyopathy. Exertional syncope may occur in these patients because of obstruction to left ventricular outflow by aortic stenosis or septal hypertrophy . Dizziness that occurs even when the patient is lying down or that is made worse by movements of the head is more likely to be of neurological origin (vertigo), although recurrent tachyarrhythmias may occasionally cause dizziness in any position. Try to decide whether the dizziness is really vertiginous (there is a sensation of movement or spinning of the surroundings or the patient’s head), or whether it is a presyncopal feeling. A family history of syncope or sudden death raises the possibility of an ion channel abnormality (long QT syndrome, Brugada syndrome or hypertrophic cardiomyopathy). Attempts should be made to find out what the diagnosis was for the affected relatives. A past history of severe structural heart disease, especially heart failure,
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR Cardiomyopathies and valvular heart disease Regardless of the status of the coronary arterial tree, both primary and secondary heart muscle disease can produce anginal pain through the imbalance of the oxygen demand and supply. Hypertrophic cardiomyopathy is a relatively common cause of angina in the presence of normal coronary arteries. Aortic stenosis is the most common valvular cause of exertional chest tightness, which is probably due to myocardial ischaemia Exertional chest pain, which may be due to right ventricular angina, is a feature of pulmonary hypertension . Syndrome X There is some confusion regarding the ‘metabolic’ and ‘cardiac’ varieties. The former is a combination of insulin resistance, obesity, pro-inflammatory state and so on, leading to raised cardiovascular risk in the sufferers. The latter is, or should be, a form of stable effort angina that can be ascribed to coronary microvascular malfunction.23 The epicardial coronary tree is normal and the diagnosis is rather difficult to make except by exclusion. Acute coronary syndromes The terminology used to describe acute coronary syndromes (ACSs) continues to evolve as clinicians attempt to adjust to the accumulating evidence of the usefulness of modern cardiac markers and the treatment implications of different results. The most recent terminology is designed to help with treatment decisions based on the earliest clinical information from the patient. This comes from the history and the ECG. When the patient’s symptoms suggest an acute coronary syndrome, the first decisions about diagnosis and treatment are based on the ECG. If there is ST elevation present in a pattern to suggest myocardial infarction, the diagnosis is of ‘ST elevation myocardial infarction’ (STEMI). If there is no ST elevation, the initial diagnosis is of ‘non-ST elevation acute coronary syndrome’ (NSTEACS).24 This elegant phrase has replaced ‘non-ST elevation myocardial infarction’ (non- STEMI). The reason is that the diagnosis of infarction cannot be made in the absence of ST elevation until cardiac marker estimations are available. The decisions about treatment, however, need to be made immediately and are based on symptoms and ECG changes.
ECHOCARDIOLOGIST IN GANGAMMA CIRCLE Mitral regurgitation A regurgitant mitral valve allows part of the left ventricular stroke volume to regurgitate into the left atrium, imposing a volume load on both the left atrium and the left ventricle. Symptoms: Dyspnoea (increased left atrial pressure); fatigue (decreased cardiac output). General signs: Tachypnoea. The pulse: Normal, or sharp upstroke due to rapid left ventricular decompression; atrial fibrillation is relatively common. Palpation: The apex beat may be displaced, diffuse and hyperdynamic if left ventricular enlargement has occurred; a pansystolic thrill may be present at the apex; a parasternal impulse (due to left atrial enlargement behind the right ventricle—the left atrium is often larger in mitral regurgitation than in mitral stenosis and can be enormous). All these signs suggest severe mitral regurgitation. Auscultation Soft or absent S1 (by the end of diastole, atrial and ventricular pressures have equalised and the valve cusps have drifted back together); left ventricular S3, due to rapid left ventricular filling in early diastole; pansystolic murmur maximal at the apex and usually radiating towards the axilla. Causes of chronic mitral regurgitation: (i) Degenerative; (ii) rheumatic; (iii) mitral valve prolapse; (iv) papillary muscle dysfunction, due to left ventricular failure or ischaemia.
SAMIKSHA HEART AND DIABETIC CARE IN YELAHANKA Echocardiographic findings in certain cardiac abnormalities It is important to be aware that modern colour flow mapping is so sensitive that small amounts of regurgitation are often detected from quite normal valves. Deciding whether these jets are significant can be difficult and requires experience. Mitral stenosis Thickening and doming of the mitral valve leaflets is visible on M mode and 2D scanning , It may be possible to measure the valve area by planimetry . Secondary changes such as left atrial size and the presence of rheumatic disease of other valves can be seen. Doppler interrogation of the jet of blood entering the left ventricle through the mitral valve will enable estimation of the valve area by a formula called the pressure half-time equation This will usually give accurate and consistent estimates of the valve area and is especially useful for serial measurements over months or years. It will also be possible to detect associated mitral regurgitation with Doppler. Mitral regurgitation and mitral valve prolapse Here the mitral valve may appear normal and abnormal co-aptation of the leaflets is not usually visible . The left atrium will appear enlarged if significant chronic MR is present, and if this is severe left ventricular dilatation will be present. If the MR is due to mitral valve
THE BEST CARDIOLOGISTS IN YELAHANKA Aortic regurgitation The incompetent aortic valve allows regurgitation of blood from the aorta to the left ventricle during diastole for as long as the aortic diastolic pressure exceeds the left ventricular diastolic pressure. Symptoms: Occur in the late stages of disease and include exertional dyspnoea, fatigue, palpitations (hyperdynamic circulation) and exertional angina. General signs: Marfan’s syndrome may be obvious. The pulse and blood pressure: The pulse is characteristically collapsing; there may be a wide pulse pressure. The neck: Prominent carotid pulsations (Corrigan’s sign). Palpation: The apex beat is characteristically displaced and hyperkinetic. A diastolic thrill may be felt at the left sternal edge when the patient sits up and breathes out. Auscultation): A2 (the aortic component of the second heart sound) may be soft; a decrescendo high-pitched diastolic murmur beginning immediately after the second heart sound and extending for a variable time into diastole—it is loudest at the third and fourth left intercostal spaces; a systolic ejection murmur is usually present (due to associated aortic stenosis or to torrential flow across a normal diameter aortic valve). Signs indicating severe chronic aortic regurgitation: Collapsing pulse; wide pulse pressure; long decrescendo diastolic murmur; left ventricular S3 (third heart sound); soft A2; signs of left ventricular failure. Causes of chronic aortic regurgitation: (i) Rheumatic (rarely the only murmur in this case), congenital; (ii) aortic root dilatation—Marfan’s syndrome, dissecting aneurysm. 8• THE PATIENT WITH A MURMUR 305 a b Valve cusps often thickened and calcified Left ventricle may be hypertrophied Ascending aorta may be dilated Systole Diastole S1 A2 P2 S1 Ejection click (Suggests congenital AS) Normal Mild S1 S1 Moderate S1 P2 A2 S1 Severe Reversed S2 Single (S2)
THE BEST CARDIOLOGIST IN YELAHANKA Mitral regurgitation A regurgitant mitral valve allows part of the left ventricular stroke volume to regurgitate into the left atrium, imposing a volume load on both the left atrium and the left ventricle. Symptoms: Dyspnoea (increased left atrial pressure); fatigue (decreased cardiac output). General signs: Tachypnoea. The pulse: Normal, or sharp upstroke due to rapid left ventricular decompression; atrial fibrillation is relatively common. Palpation: The apex beat may be displaced, diffuse and hyperdynamic if left ventricular enlargement has occurred; a pansystolic thrill may be present at the apex; a parasternal impulse (due to left atrial enlargement behind the right ventricle—the left atrium is often larger in mitral regurgitation than in mitral stenosis and can be enormous). All these signs suggest severe mitral regurgitation. Auscultation Soft or absent S1 (by the end of diastole, atrial and ventricular pressures have equalised and the valve cusps have drifted back together); left ventricular S3, due to rapid left ventricular filling in early diastole; pansystolic murmur maximal at the apex and usually radiating towards the axilla. Causes of chronic mitral regurgitation: (i) Degenerative; (ii) rheumatic; (iii) mitral valve prolapse; (iv) papillary muscle dysfunction, due to left ventricular failure or ischaemia. Mitral valve prolapse (systolic-click murmur syndrome) This syndrome can cause a systolic murmur or click, or both, at the apex. The presence of the murmur indicates that there is some mitral regurgitation present. Auscultation: Systolic click or clicks at a variable time (usually mid-systolic) may be the only abnormality audible, but a click is not always audible; systolic
BEST DIABETOLOGISTS IN HEBBALA BANGALORE Diabetes Type 1 and type 2 diabetes and impaired glucose tolerance (IGT) are associated with an increased risk of coronary disease, peripheral vascular disease and cerebrovascular disease.21 Diabetics have a two- to threefold risk of coronary disease at all ages and those with IGT have a 1.5-fold risk. Diabetes is a stronger risk factor for women (3.3 times) than for men (1.9 times). The excess risk for type 1 patients is largely confined to those with diabetic renal disease. All type 2 patients are at increased risk.22 Diabetes is thought to increase coronary heart disease because: n increased insulin levels result in increased hepatic synthesis of LDL and triglycerides, causing a mixed dyslipidaemia n insulin resistance, which is characteristic of type 2 diabetes, is associated with numerous other cardiovascular risk factors: dyslipidaemia, hypertension, endothelial dysfunction and microalbuminuria n hyperglycaemia itself may cause endothelial damage n glycosylated LDL may be more atherogenic than non-glycosylated LDL. Table 1.12 Glucose tolerance, current WHO definitions (venous plasma glucose) Fasting glucose 2-hour post-glucose load (mmol/L) Normal glucose regulation < 6.0 < 7.8 Impaired fasting glucose 6.1–6.9 < 7.8 Impaired glucose tolerance < 7.0 7.8–11.0 Diabetes > 7.0 > 11.1 16 PRACTICAL CARDIOLOGY Glycaemic control The UKPDS Trial has shown a very significant reduction in the microvascular complications of diabetes with improved glycaemic control but the improvement in macrovascular complications did not quite reach significance. Nevertheless, the UKPDS trialists estimate that each 1% reduction in HbA1c leads to a 14% reduction in cardiovascular risk. Diabetics tend to have more diffuse coronary disease. shows a diffusely diseased right coronary artery from a type 2 diabetic patient before and after coronary stenting . Coronary artery surgery involves a higher risk for diabetics, and graft disease and progression of native disease occur earlier in these patients. Nevertheless, diabetics probably have a better prognosis after surgical revascularisation than after angioplasty because of their higher risk of restenosis following angioplastY
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