Cardiophile MD Archive » General

Coronary calcium scoring

Johnson Francis — Tue, 25 May 2010 15:44:46 +0000

Coronary calcium scoring is used to indirectly assess coronary atherosclerosis. Calcification occurs in atherosclerotic plaques and progresses with the severity of the process and is not seen in normal arteries. There is some correlation between the amount of calcification and the severity of coronary artery disease, though it is not a perfect one to one relationship. It is also uncertain whether calcification correlates with the chance of plaque rupture and consequent acute coronary syndromes. Though calcium can be related to the plaque burden, it may not be directly correlated with luminal stenosis as the plaque often grows abluminally, producing positive remodeling of the vessel wall.

It may seem that calcified plaques are likely to be stable and unlikely to rupture and predispose to acute coronary events. But those with higher calcium scores have a larger plaque burden, some of which may be calcified while others may not be. It is reasonable to assume that those with higher plaque can have some unstable plaques prone for rupture as well. This is how the coronary score gains importance as a risk predictor.

Calcium score between 100 and 400 project a relative risk ratio of 4.3 compared to those with no detectable coronary calcium (low risk group with calcium score = 0). In those with high calcium scores of 400 to 1000, the relative risk ratio is 7.2 and that for very high scores, greater than 1000, the relative risk ratio is 10.8. Calcium score is rather 100% specific for coronary plaques while it is not specific for obstructive coronary artery disease. But higher calcium scores increase the probability of having significant coronary stenosis.

Vernakalant for conversion of atrial fibrillation

Johnson Francis — Tue, 18 May 2010 11:40:25 +0000

Vernakalant hydrochloride is a novel anti arrhythmic agent which is atrial selective, blocking the early activating potassium channel and frequency dependent sodium channel. It has a half life of two to three hours. In animal studies, it has been shown to selectively prolong the atrial refractory period without affecting the ventricular refractory period. In a phase 3 trial patients with short duration atrial fibrillation had a 51.7% conversion to sinus rhythm with a median time of eleven minutes. There were 145 patients on vernakalant and 75 patients on placebo in the group with short duration atrial fibrillation. Most common side effects noted were transient dysgeusia and sneezing with vernakalant. Three patients had significant adverse events in the form of hypotension, complete heart block and cardiogenic shock. But the complete heart block and cardiogenic shock occurred after electrical cardioversion as vernakalant infusion had been stopped due to hypotension. In contrast to the good efficacy in atrial fibrillation of short duration, only six of the seventy six patients (7.9%) patients with long duration atrial fibrillation had conversion with vernakalant. Atrial flutter may occur with vernakalant needing AV nodal blocking drugs for rate control of the ventricular rate. Vernakalant seems to have a lower risk for torsades de pointes than ibutilide, the other drug for conversion of atrial fibrillation.

Management of primary pulmonary hypertension

Johnson Francis — Fri, 14 May 2010 10:17:06 +0000

Primary pulmonary hypertension is a condition with a guarded prognosis and most often a limited survival. Various agents have been tried in the management of primary pulmonary hypertension, with limited efficacy. Anticoagulants have been used for a long time and should be maintained at therapeutic INR (internationally normalized ratio) levels of prothrombin time to document effective dosing. Digoxin, diuretics and oxygen supplementation have a role in those with heart failure. Calcium channel blockers have been used in fairly high doses for the treatment of primary pulmonary hypertension. Nifedipine and diltiazem are the two important agents, with latter being preferred when the heart rate is on the higher side, due to the response of nifedipine producing reflex tachycardia and diltiazem producing bradycardia. Ideally a response to vasodilators have to be documented before starting these, with epoprostenol or nitric oxide. Calcium channel blockers are not to be given if there are features of right ventricular dysfunction or failure as these agents have negative inotropic effects which can worsen the ventricular dysfunction.

Prostacyclin analogues like epoprostenol which is given intravenously, treprostinil which may be given intravenously, subcutaneously and iloprost which is given by nebulization are other agents found useful in the management of primary pulmonary hypertension. Oral phosphodiesterase 5 (PDE 5) inhibitors like sildenafil and tadalafil also have beneficial effects in primary pulmonary hypertension. The latest addition to the therapeutic armamentarium are oral endothelin antagonists bosentan and ambrisentan.

Aliskiren an antihypertensive for use in chronic kidney disease (CKD)

Johnson Francis — Fri, 14 May 2010 00:44:03 +0000

Angiotensin-converting enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) are widely used antihypertensive agents which block the renin-angiotensin-aldosterone system (RAAS). They also have a role in delaying the progression of chronic kidney disease. By they have an inherent disadvantage of feed back increase in plasma renin activity. Aliskiren is novel agent which inhibits renin, the first limb of the RAAS. Aliskiren may have more renoprotective effects compared to ACE inhibitors and ARBs. Studies in animals have shown improved surivival and decreased renal injury with aliskiren. It has been shown that it can be safely used in chronic kidney disease (CKD) in humans for control of hypertension. Aliskiren has also been shown to decrease albuminuria when added to losartan in patients with early diabetic nephropathy in a randomized clinical trial. What remains to be proved are the effects of aliskiren on the hard renal end points and cardiovascular events. Aliskiren has also been reported to cause hyperkalemia like the ACE inhibitors and ARBs, especially when combined with agents like spironolactone, in the presence of unrecognized underlying CKD. Renin is the rate limiting step in RAAS and inhibition of renin with direct renin inhibitors (DRIs) seems to have a potential in preventing the progression of CKD. A combination of aliskiren with ACEI or ARB may be better tolerated than a combination of ACEI with an ARB. We need more large scale randomised clinical trials for further evaluating the benefits and disadvantages if any, of aliskiren as a novel renoprotective agent.

Recently FDA has issued a safety warning regarding the rare possibility of angioedema with aliskiren, which can occur in those with or without a history of angioedema with ACE inhibitors. This can be rarely fatal if involving the upper airway and needs close observation and immediate treatment. http://www.fda.gov/Safety/MedWatch/SafetyInformation/ucm215535.htm

Fetal and transitional circulation

Johnson Francis — Fri, 07 May 2010 05:35:27 +0000

Since the fetal lungs are not functional, the respiratory gas exchange occurs in the placenta. Blood flow to the lungs is very little in the fetal circulation and the pulmonary vascular resistance is very high. Blood from the placenta with oxygenation leaves by the umbilical veins and gets shunted by the ductus venosus in the liver. Thus the blood reaches the inferior vena cava and into the right atrium. From the right atrium, most of the oxygenated blood is shunted across the foramen ovale into the left atrium. Blood from the left atrium reaches the left ventricle, with a minimal contribution from the pulmonary veins with scanty blood flow. Thus the oxygenated blood is pumped out of the left ventricle into the aorta and hence to the brain and upper extremities. Blood from the superior vena cava reaching the right atrium is streamed towards the right ventricle and into the pulmonary artery. Most of this deoxygenated blood gets shunted across the ductus arteriosus into the descending aorta as there is no role for the lungs in oxygenation and hence very little pulmonary blood flow. The descending aorta thus has less saturated blood which reaches the placenta through the umbilical artery. The lower extremities also get the less saturated blood. But the fetal circulation ensures that the developing brain gets a higher saturation of oxygen. Fetal hemoglobin has a higher oxygen binding affinity than the adult hemoglobin and oxygen dissociation curves are different.

Transition from fetal circulation after birth

Several changes occur after birth during the transition from the fetal circulation. The umbilical cord is tied and the umbilical arteries and vein become non functional. Pulmonary vascular resistance drops markedly from the first breath and continues to fall for weeks as the musculature of the pulmonary vessel regress. Hence pulmonary blood flow increases markedly. Right atrial pressure decreases and left atrial pressure increases, leading to closure of the valvular foramen ovale which permits only blood flow from the right atrium to the left atrium. The increase in the oxygen levels acts as a strong stimulus for the closure of the ductus arteriosus. Ductus venosus also closes. As a consequence of the decrease in pulmonary vascular resistance and fall in right sided pressures, right ventricle starts regressing. The levels of fetal hemoglobin also gradually drops.

Coronary artery disease risk locus on chromosome 9p21

Johnson Francis — Thu, 06 May 2010 01:56:47 +0000

Chromosome 9p21 single nucleotide polymorphisms (SNPs) have been associated with risk for coronary artery disease. Transcripts EU741058 and NR_003529 of annotated antisense non-coding RNA in the INK4 locus (ANRIL) are involved in the risk of coronary artery disease. The association of chromosome 9p21 and coronary artery disease has been shown several independent populations. A recent study published in Circulation. 2009;120:2062-8 prospectively evaluated the risk of development of sudden cardiac death as well. They determined genotypes for rs10757274 for 492 sudden and/or arrhythmic deaths and 1460 matched controls. The age adjusted odds ratio for sudden cardiac death was 1.21 for every copy of the G allele at rs10757274. This study was in persons of European ancestry from six prospective cohort studies.

Another study evaluating perioperative myocardial injury in patients undergoing cardiac surgery also found that common genetic variants on chormosome 9p21 are associated with perioperative myocardial injury. Chromosome 9p21.3 region has also been implicated as a major risk locus in atherosclerotic stroke.

Paget-Schrotter syndrome

Johnson Francis — Wed, 05 May 2010 17:12:33 +0000

Paget-Schrotter syndrome is the spontaneous thrombosis of the deep veins of the upper limb – axillary or subclavian vein.The syndrome was described independently by Von-Schrotter in 1884 and by Paget in 1875. Paget-Schrotter syndrome is also known as effort thrombosis because it is often associated with activities involving hyperabduction of the upper limbs. Sudden jerky movements cause the axillary vein to be crushed between the clavicle and the first rib. This can damage the intima of the vein and initiate thrombosis. The syndrome is also associated with thoracic outlet syndrome due to similar compressive reasons. Painful swelling of the limb is an important manifestation of the Paget-Schrotter syndrome. The diagnosis is confirmed by compression ultrasonography or venography. Treatment is by thrombolysis and anticoagulation. Surgical options are needed only for those with persistent symptoms of thoracic outlet compression. Important differential diagnoses include lymphangitis, lymphatic obstruction and intramuscular hemorrhage.

Post-thrombotic syndrome

Johnson Francis — Wed, 05 May 2010 17:01:17 +0000

Post-thrombotic syndrome develops after a deep vein thrombosis. Post-thrombotic syndrome is characterised by swelling, stasis dermatitis, ulceration and venous claudication of the affected limb. Treatment of deep vein thrombosis reduces the risk of development of post-thrombotic syndrome. The prevention of post-thrombotic syndrome is one of the important aims of treatment of deep vein thrombosis, the other important aim being the prevention of pulmonary embolism. Post-phlebitic syndrome is another name used to describe the post-thrombotic syndrome. Compression stockings are useful in the treatment of post-phlebitic syndrome. About one fifth to one half of patients develop post-thrombotic syndrome within one to two years of a symptomatic deep vein thrombosis. Venous ulcers may develop in 5-10% of cases. Documenting incompetence of the venous valves is useful in confirming the diagnosis in symptomatic individuals. The role of thrombolysis and venoactive drugs in preventing post-thrombotic syndrome needs evaluation.

Anatomy of the mitral valve

Johnson Francis — Wed, 28 Apr 2010 00:42:40 +0000

Anatomical considerations of the mitral valve are important while considering mitral valve repair either surgically or by percutaneous trans catheter techniques. The mitral valve complex consists of the mitral annulus, mitral valve leaflets, the chordae tendinae and the papillary muscles. The mitral leaflets are the anterior and posterior leaflets.

Scallops of the mitral valve

The posterior leaflet has three scallops named P1, P2 and P3. The commissures of the mitral valve are the anterolateral and the posteromedial commissures. The papillary muscles are the anterolateral and the posteromedial papillary muscles. The P1 scallop is near the anterolateral commissure and the P3 scallop is near the posteromedial commissure, with the P2 scallop in the middle. They are also called the lateral, central and medial scallops. Though the anterior leaflet does not have well defined scallops like the posterior leaflets, there are corresponding named segments known as A1, A2 and A3.

Primary, secondary and tertiary chordae

The chordae tendinae are of three types – primary, secondary and tertiary. Primary chordae attach to the tips of the mitral leaflets while the secondary chordae connect the rough zone of the leaflets to the papillary muscles. The secondary chords are are also known as strut chords. The tertiary chordae are attached to the basal region of the mitral leaflets and connect to the ventricular free wall. The tensing of the chordopapillary system during systole has an important role in the competence of the mitral valve in preventing regurgitation.

Echocardiogram with video in coronary artery disease with left ventricular dysfunction and additional aortic regurgitation

Johnson Francis — Mon, 12 Apr 2010 01:17:35 +0000

M-mode echocardiogram at mitral valve level

M-mode echocardiogram at the level of mitral valve showing the early diastolic E wave and the atrial systolic A wave. The left ventricle (LV) is dilated and the left ventricular posterior wall (LVPW) contractions are reduced. The distance from the E point of the mitral valve and interventricular septum (IVS) is increased due to the poor excursions of the mitral valve on opening and the dilated left ventricle. The overall left ventricular function is reduced and there is regional wall motion abnormality suggestive of coronary artery disease.

Doppler tracing in aortic regurgitation

The continuous wave Doppler cursor is seen along the left ventricular outflow tract and the aorta. The upper panel shows the two dimensional image in the apical five chamber view showing all four cardiac chambers and the aorta. The colour flow mapping overlay shows the turbulent multicoloured mosaic jet in the left ventricular outflow tract just beneath the aortic valve suggestive of aortic regurgitation. The diastolic mitral flow is seen as a red colour in just beyond the mitral valve, in the left ventricle. The lower panel shows the Doppler tracing in aortic regurgitation (AR). The AR jet is upwards as it moves towards the transducer kept at the left ventricular apex. The small tracing below the baseline is the forward aortic flow, which is denser as it covers the whole forward cardiac output. The retrograde flow due to aortic regurgitation is fainter because the volume of aortic regurgitation is not severe.

Pressure half time in aortic regurgitation

Measurement of pressure half time in aortic regurgitation is used in assessing the severity of aortic regurgitation. It is inversely related to the severity of aortic regurgitation. The beginning of the diastolic tracing corresponds to the pressure difference between the aorta and the left ventricle in early diastole while the end of the tracing represents the end diastolic gradient. When the regurgitation is severe, there is rapid equalisation of the aortic and ventricular diastolic pressures. This causes the pressure half time to be shorter. Pressure half time is the time taken for the pressure difference to fall by half. In this case the pressure half time (P1/2) is high (712 msec) as the aortic regurgitation is not severe.

Echocardiographic video showing regional wall motion abnormalities, left ventricular dysfunction and additional aortic regurgitation, which is not related to the coronary artery disease which caused the regional wall motion abnormalities and left ventricular dysfunction. Aortic regurgitation is seen as a multicoloured mosaic jet into the left ventricular outflow tract from the aorta in diastole, both in the parasternal long axis view and the apical five chamber view. The jet length and width are not large since the regurgitation is not severe. Parasternal long axis view also shows the dilated left ventricle with diminshed contractions of the posterior wall. The opening excursions of the mitral valve are reduced due to the left ventricular dysfunction and low output state. The separation between the maximum excursion of the mitral valve and the interventricular septum are increased due to both the left ventricular dilatation and the reduced opening motion of the mitral valve. The apical five chamber view shows the dilated left ventricle with a bulge of the mid and distal interventricular septum towards the right ventricular cavity, as a manifestation of the underlying coronary artery disease.