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SAMIKSHA HEART AND DIABETIC CARE ''CONNECTIVE TISSUE DISORDERS'' ''Marfan Syndrome'' Marfan syndrome is a systemic connective tissue disorder with a frequency of 2 to 3 in 10, 000. The disorder is characterized by manifestations involving the cardiovascular, skeletal, and ocular systems. Current diagnostic criteria are based on involvement of above organ systems and family history. Cardiovascular manifestations include mitral valve prolapse, progressive aortic root enlargement, and ascending aortic aneurisms, possibly leading to aortic regurgitation, dissection, or rupture. Some characteristic skeletal manifestations of this syndrome include disproportional increase of linear bone growth resulting in malformations of the digits (arachnodactyly), craniofacial abnormalities, pectus excavatum/carinatum, and scoliosis. A common ocular involvement is severe myopia and lens dislocation in one or both eyes (ectopia lentis). Marfan syndrome is an autosomal dominant disorder caused by fibrillin-1 gene mutations encoding for the extracellular matrix protein fibrillin (Fbn-1). Fibrillin is an integral component of both elastic and nonelastic connective tissue. The mechanism of fibrillin mutation in Marfan syndrome remains unclear. However, animal models of Fbn-1 have demonstrated a role of TGF-beta signaling. In some patients with phenotypes similar to Marfan syndrome but without fibrillin- 1 gene mutations, TGF-beta receptor mutations have been identified, suggesting a significant role of TGF-beta pathway in the pathogenesis of Marfan syndrome features. Aortic root involvement remains the leading cause of death in patients with Marfan syndrome. Echocardiography is recommended to routinely screen and to follow aortic root dilation. In addition, all first-degree relatives of the family should have screening echocardiography. Patients should be advised against strenuous exercises. Medical therapy for Marfan syndrome includes beta-blockers to reduce myocardial contractility and pulse pressure. Animal models of Marfan syndrome have demonstrated a possible benefit of losartan in preventing progression of the disease by inhibiting the TGF-beta pathway, and this therapy is the subject of an active clinical trial. Elective aortic root replacement remains the therapy of choice once the aortic root becomes significantly enlarged. Marfan patients who become pregnant need to be counseled not only about the 50% chance of transmitting the disease but also the substantially increased risk of aortic rupture/dissection during and after pregnancy. Important components of Marfan syndrome counseling are consideration of contraception and pregnancy management. Loeys-Dietz Syndrome Recently, an aortic aneurysm syndrome has been identified with TGF-beta receptor mutations. Loeys-Dietz syndrome is an autosomal dominant condition with a characteristic triad of arterial tortuosity/aneurysm, hypertelorism, and bifid uvula or cleft palate. There is significant overlap with Marfan syndrome, and the management is similar in terms of cardiovascular manifestation. Early, elective, surgical intervention should be considered in patients with significant aneurysmal dilation of the aorta. Some clinicians have argued for much earlier surgical intervention for the dilated aorta in this condition, compared with Marfan syndrome, since there appears to be a much greater risk of rupture and dissection at earlier ages and smaller aortic sizes. Pregnancy counseling is also an integral part of therapy. Ehlers-Danlos Syndrome Ehlers-Danlos syndrome is a group of disorders that affect connective tissue development due to defects in collagen and connective tissue biosynthesis. Prevalence of the disease is about 1 in 400, 000 people in the United States. Cardiac manifestations include spontaneous rupture of medium to large sized arteries including the aorta. Frequently, extracardiac presentations include hyperextensible skin and hypermobile joints. To date, 11 types of the disorder have been recognized, but collagen defects have been described in only 6 types. Although all types of Ehlers-Danlos syndrome affect the joints and the skin, clinical features vary by type. Different features characterize each type of the syndrome. Type IV carries the poorest prognosis, especially due to spontaneous ruptures of arteries and organs. Extreme caution needs to be taken if surgical intervention is needed due to weakened connective tissue structures. Many genes, including ADAMTS2, COL1A1, COL1A2, COL3A1, COL5A1, COL5A2, PLOD1, and TNXB, have been implicated in the pathogenesis of Ehlers- Danlos syndrome, but the predominant cardiovascular concern exists in the Type IV vascular form of Ehlers-Danlos associated with mutations in the COL3A1 gene and aortic dilation/aneurysms. Other less commonly associated anomalies include ventricular septal defect, patent ductus arteriosus, bicuspid pulmonic valve, and Ebstein’s anomaly. Bicuspid aortic valve has been shown to demonstrate familial clustering. However, identifying culprit genes have been difficult due to variable penetrance and the common nature of the disorder.
samiksha heart and diabetic care new town yelahanka banglore The Evaluation of the Cause of Heart Failure: The History History to include inquiry regarding: Hypertension Diabetes Dyslipidemia Valvular heart disease Coronary or peripheral vascular disease Myopathy Rheumatic fever Mediastinal irradiation History or symptoms of sleep-disordered breathing Exposure to cardiotoxic agents Current and past alcohol consumption Smoking Collagen vascular disease Exposure to sexually transmitted diseases Thyroid disorder Pheochromocytoma Obesity Family history to include inquiry regarding: Predisposition to atherosclerotic disease (Hx of MIs, strokes, PAD) Sudden cardiac death Myopathy Conduction system disease (need for pacemaker) Tachyarrhythmias Cardiomyopathy (unexplained HF) Skeletal myopathies
samiksha heart and diabetic care new town yelahanka banglore The Evaluation of the Cause of Heart Failure: The History History to include inquiry regarding: Hypertension Diabetes Dyslipidemia Valvular heart disease Coronary or peripheral vascular disease Myopathy Rheumatic fever Mediastinal irradiation History or symptoms of sleep-disordered breathing Exposure to cardiotoxic agents Current and past alcohol consumption Smoking Collagen vascular disease Exposure to sexually transmitted diseases Thyroid disorder Pheochromocytoma Obesity Family history to include inquiry regarding: Predisposition to atherosclerotic disease (Hx of MIs, strokes, PAD) Sudden cardiac death Myopathy Conduction system disease (need for pacemaker) Tachyarrhythmias Cardiomyopathy (unexplained HF) Skeletal myopathies
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin . Right ventricular hypertrophy The main criteria fSAor detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QRS) In congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
HEART DOCTORS IN BETTAHALASUR, BANGALIREHypertension and pregnancy Hypertension is the most common complication of pregnancy and remains an important cause of maternal and fetal mortality and morbidity. Hypertension in pregnancy can be classified as follows: 1 Chronic: existing hypertension with or without proteinuria. 2 Pre-eclampsia or eclampsia: proteinuria (> 300 mg/day) as well as new hypertension. Note that oedema is no longer part of the definition. 3 Pre-eclampsia in the context of existing hypertension: blood pressure higher than before pregnancy. 4 Gestational hypertension: new hypertension > 140/90 at least twice and after week 20 of pregnancy; no proteinuria. For most patients with existing hypertension the problem is just the blood pressure elevation. Pre-eclampsia, on the other hand, is a serious systemic disorder. It seems related to endothelial dysfunction due to failure of normal placental perfusion and the release of an unknown endothelial toxin. This causes vasospasm, reduced organ perfusion and eventually activation of the coagulation cascade. Superimposed pre-eclampsia occurs in up to 35% of women with pre-existing hypertension. These women are also at risk of abruptio placentae and cerebral haemorrhage. The fetus may also be affected by prematurity and there is an increased risk of still birth. Gestational hypertension does not involve proteinuria and if blood pressure returns to normal within 12 weeks of delivery, it is called
CARDIAC CENTERS IN YELAHANKA NEW TOWN BANGALORE ST segment There are two aspects to report: depression and elevation. Depression The ST segment is said to be abnormal if it slopes down 1 mm or more from the J point—the end of the QRS complex (downsloping depression)—or is depressed 1 mm or more horizontally (plane depression). Depression of the J point itself may be normal, especially during exercise, but this upsloping ST depression should return to the isoelectric line within 0.08 seconds. The isoelectric line is defined as the PR or TP segment of the ECG . ST depression may be due to ischaemia, the effect of digoxin, hypertrophy and so on. Elevation ST elevation of up to 3 mm may be normal in V leads (especially the right), and up to 1 mm may be normal in limb leads. This ST elevation is called early repolarisation syndrome or pattern. Otherwise ST elevation may mean an acute myocardial infarction where it is said to represent a current of injury. Pericarditis also causes ST elevation but unlike infarction is usually associated with concave upwards elevation. hypertrophy and conduction defects like LBBB can be associated with ST elevation in leads where the QRS is mostly negative. T waves The T wave is always inverted in lead aVR and often in L3 and V1–V2, and in aVL if the R wave is less than 5 mm tall. Inversion and flattening are common and non-specific findings. Deep (> 5 mm) symmetrical and persistent (days to weeks) inversion is consistent with infarction; broad, ‘giant’ inversion may follow syncope from any cause including cerebrovascular accidents. Like the ST segment, the T wave tends to be directed opposite to the main QRS deflection in conduction defects (e.g. LBBB), VEBs or ventricular hypertrophy (where it is described as secondary ST/T changes or strain pattern). Tall peaked T waves are most often seen as a reciprocal change to inferior or posterior infarcts. They are classically seen in patients with hyperkalaemia. Broader large T waves are seen in early (‘hyperacute’) infarction and sometimes in cerebrovascular accidents. While not diagnostic by themselves (T waves never are), when they are associated with modest ST elevation (especially in V3) and reciprocal depression in the inferior leads, they indicate infarction or ischaemia. When these changes evolve over time they are even more specific for infarction . A U wave may be prominent in patients with hypokalaemia, LVH and bradycardia. Isolated U inversion is a specific but insensitive sign of coronary disease. 54 PRACTICAL CARDIOLOGY ECG reports Reports should be short and stereotyped, with the description clearly separated from the comment. It is a good general strategy to under-report, especially for a beginner. It is generally wiser to state ‘inferior Q waves noted’ or ‘non-specific ST/T changes’ than to indulge in speculation on possible or probable infarction or ischaemia. ECG labels tend to have serious employment and insurance implications. On the other hand, specific questions on the request form must be addressed, since they constitute the reason for taking the ECG in the first place.
the best cardiologists in yelahanka new town bangalore Miscellaneous conditions Chamber hypertrophy Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present ) Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin . Right ventricular hypertrophy The main criteria for detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QRS) . In congenital heart disease conduction defects often come to obscure the hypertrophy patterns. An atrial (AAI) pacemaker in a patient with anterior myocardial infarction of uncertain age. There is sensing (inhibition) only after some native or paced P waves. The pacemaker captures the atria whenever the latter are not refractory: there is no failure to pace. The middle capture beat is earlier than the other two and has a longer PR interval and aberrant RBBB-type ventricular conduction. This is a pacemaker sensing problem. Reprogramming may enable the pacemaker to sense a smaller atrial amplitude and be inhibited correctly. A DDD pacemaker in trouble: there is no atrial capture and the ventricular complexes are capturing the atria on their own. The retrograde P wave interrupts the T wave and triggers another paced QRS whose retrograde conduction is blocked by the original retrograde P wave. Were it not for this block, an endless loop re-entry (paced) tachycardia would occur. The paced complexes have the typical LBBB/left-axis deviation expected from right ventricular apical pacing. Failure to capture may mean the lead has been displaced or that scarring has developed between the tip of the lead and the myocardium. Sometimes, reprogramming an increase in the output of the pacemaker will fix the problem. a = atrial pacing spike (not followed by a P wave); b = ventricular pacing spike (produced after the atrial spike after a programmed AV delay and followed by a paced ventricular beat); c = retrograde P wave following ventricular paced beat; d = pause caused by blocked retrograde conduction of the previo A DDD or VDD pacemaker with intermittent failure to pace. A 4:3 pacemakerventricular block results in trigeminy even though normal sinus rhythm continues throughout. The normal
the best cardiologists in yelahanka new town bangalore Miscellaneous conditions Chamber hypertrophy Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present ) Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin . Right ventricular hypertrophy The main criteria for detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QRS) . In congenital heart disease conduction defects often come to obscure the hypertrophy patterns. An atrial (AAI) pacemaker in a patient with anterior myocardial infarction of uncertain age. There is sensing (inhibition) only after some native or paced P waves. The pacemaker captures the atria whenever the latter are not refractory: there is no failure to pace. The middle capture beat is earlier than the other two and has a longer PR interval and aberrant RBBB-type ventricular conduction. This is a pacemaker sensing problem. Reprogramming may enable the pacemaker to sense a smaller atrial amplitude and be inhibited correctly. A DDD pacemaker in trouble: there is no atrial capture and the ventricular complexes are capturing the atria on their own. The retrograde P wave interrupts the T wave and triggers another paced QRS whose retrograde conduction is blocked by the original retrograde P wave. Were it not for this block, an endless loop re-entry (paced) tachycardia would occur. The paced complexes have the typical LBBB/left-axis deviation expected from right ventricular apical pacing. Failure to capture may mean the lead has been displaced or that scarring has developed between the tip of the lead and the myocardium. Sometimes, reprogramming an increase in the output of the pacemaker will fix the problem. a = atrial pacing spike (not followed by a P wave); b = ventricular pacing spike (produced after the atrial spike after a programmed AV delay and followed by a paced ventricular beat); c = retrograde P wave following ventricular paced beat; d = pause caused by blocked retrograde conduction of the previo A DDD or VDD pacemaker with intermittent failure to pace. A 4:3 pacemakerventricular block results in trigeminy even though normal sinus rhythm continues throughout. The normal
Cardiologist in Chikkajala, Bangalore • Electronic pacemakers Pacemakers come as temporary or permanent, fixed-rate (although only if they are faulty these days), demand or rate-responsive, atrial, ventricular, biventricular or dual chamber, unipolar or bipolar and as a combination of many of these features. In routine ECG reporting the pacemaker’s exact programming is not usually known, but it is still possible to diagnose the pacemaker type Acute inferolateral infarction with LBBB. Although ST elevation and depression in the limb leads are suggestive, the more discrete elevation in V6 proves the diagnosis (arrows). Within hours, it disappeared and all that was left were primary T wave changes in the inferior leads ). The same patient as in , showing residual primary T wave changes in the inferior leads 90 PRACTICAL CARDIOLOGY Pathological Q waves in all the LV leads in a 90-year-old man with known old anterior infarction Table 3.1 The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) generic (NBG) pacemaker codes Position I II III IV V Category Chamber(s) paced Chamber(s) sensed Response to sensing Programmability, rate modulation Anti- tachyarrhythmia function(s) O = none A = atrium V = ventricle D = dual (A + V) O = none A = atrium V = ventricle D = dual (A + V) O = none T = triggered I = inhibited D = dual (D + I) O = none P = simple programmable M = multiprogrammable C = communicating R = rate modulation O = none P = pacing (antitachyarrhythmia) S = shock D = dual (P + S) Manufacturers’ designation only S = single (A or V) S = single (A or V) Note: positions I–III are used exclusively for anti-bradyarrhythmia function. Source: and the all-important capacity to sense the native complexes and pace the appropriate chambers. An international letter code has evolved for describing pacemaker types, shown in Table 3.1. Thus: n VVI = ventricular pacing and sensing, inhibition (in response to sensing)—the pacemaker is inhibited and produces no impulse when it senses a ventricular impulse n AAI = atrial pacing and sensing 3• AN OVERVIEW OF CLINICAL ELECTROCARDIOGRAPHY 91 n VOO = fixed-rate (asynchronous) ventricular pacing, no sensing—this is used for pacemaker testing and is the usual response of a pacemaker when a magnet is placed over it; modern pacemakers are always demand (inhibited) devices n DDD = atrial and ventricular (dual) sensing and pacing n DDDR = same as universal (DDD) pacemaker, with rate-responsiveness—the device will change its pacing rate in response to the patient’s physical activity n VDD = ventricular pacing with dual-chamber sensing (through a single lead). The above codes include the implantable cardioverter-defibrillators. ‘Failed pacemaker’ is not a proper or complete diagnosis. Failure may be intermittent or complete and involve sensing or capture (pacing), or both. A few examples are shown in More examples and details of the pacemaker syndrome and arrhythmias Miscellaneous conditions Chamber hypertrophy Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present ). Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin Right ventricular hypertrophy The main criteria for detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QR congenital heart disease conduction defects often come to obscure the hypertrophy patterns.
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