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THE BEST CARDIOLOGISTS IN YELAHANKA Second-degree AV block There are two basic types of second-degree AV block: AV nodal Möbitz type I heart block, and the more distal and more sinister Möbitz type II heart block. Möbitz type I heart block is much more common. In Möbitz type I block the PR interval lengthens progressively with each cardiac cycle, until an atrial wave is not conducted. There is recovery of conduction and the next a wave is conducted with a shorter interval and the cycle begins again. The QRS complex is narrow (unless associated with pre-existing BBB). The increment is largest between the first and second conducted P wave, and the PR interval continues to increase by less and less until a P wave is dropped. Möbitz type II heart block is almost always associated with a BBB , since its origin is intraventricular (below the AV node), and it tends to lapse suddenly into extreme bradycardia or asystole. It tends to be over-diagnosed, especially in the setting of 2:1 AV block . There is no lengthening of the PR interval before an atrial wave is not conducted. At times, atropine or exercise can demonstrate the site of the block, by increasing the block from 2:1 to a higher grade when the underlying mechanism is Möbitz II. Conversely, Wenckebach conduction may improve to 3:2 or better. For a distinction to be made between Möbitz type I and Möbitz type II, at least two consecutively conducted P waves have to be evaluated. This is impossible in 2:1 conduction (block) and can only be reported as 2:1 AV block (Fig 3.12). Yet this is very commonly reported as Möbitz type
CARDIOLOGIST IN YELAHANKA SECOND DEGREE AV BLICK There are two basic types of second-degree AV block: AV nodal Möbitz type I (Wenckebach) heart block, and the more distal and more sinister Möbitz type II heart block. Möbitz type I heart block is much more common. In Möbitz type I block the PR interval lengthens progressively with each cardiac cycle, until an atrial wave is not conducted. There is recovery of conduction and the next a wave is conducted with a shorter interval and the cycle begins again. The QRS complex is narrow (Fig 3.10) (unless associated with pre-existing BBB). The increment is largest between the first and second conducted P wave, and the PR interval continues to increase by less and less until a P wave is dropped. Möbitz type II heart block is almost always associated with a BBB (Fig 3.11), since its origin is intraventricular (below the AV node), and it tends to lapse suddenly into extreme bradycardia or asystole. It tends to be over-diagnosed, especially in the setting of 2:1 AV block (Fig 3.12). There is no lengthening of the PR interval before an atrial wave is not conducted. At times, atropine or exercise can demonstrate the site of the block, by increasing the block from 2:1 to a higher grade when the underlying mechanism is Möbitz II. Conversely, Wenckebach conduction may improve to 3:2 or better. For a distinction to be made between Möbitz type I and Möbitz type II, at least two consecutively conducted P waves have to be evaluated. This is impossible in 2:1 conduction (block) and can only be reported as 2:1 AV block (Fig 3.12). Yet this is very commonly reported as
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.
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
THE BEST DIABETOLOGISTS IN HSR LAY OUT 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.
THE BEST DIABETOLOGISTS IN HSR LAY OUT 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.
Types of Diabetes Learn about Diabetes You can learn how to take care of your diabetes and prevent some of the serious problems diabetes can cause. The more you know, the better you can manage your diabetes... Share this booklet with your family and friends so they will understand more about diabetes. Also make sure to ask your health care team any questions you might have.''
HEART SPECIALISTS IN SILKBOARD Complex congenital heart disease: conduits Anatomy and physiology Babies with a very abnormal right ventricular outflow tract such as pulmonary atresia can have a conduit fashioned to direct blood from the systemic veins more directly to the pulmonary arterial circulation or from a systemic artery to the pulmonary circulation. These conduits are made from veins or occasionally from Gortex. 368 PRACTICAL CARDIOLOGY Complications Conduits of all types have a limited life and tend to deteriorate after 10 years. These patients are also at risk of ventricular arrhythmias and heart block. Follow-up Patients need regular expert echocardiography to assess the conduit function. The conduit may deteriorate significantly before symptoms occur. Further treatment Conduit deterioration is usually an indication for further surgery although it can occasionally be treated with balloon dilatation. Pregnancy and contraception Pregnancy is well tolerated in patients with good conduit function. There are no particular problems with contraception. Sports Patients should avoid competitive and contact sports.
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.
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