Antiplatelet drugs The most important antiplatelet drugs are: Cyclooxygenase inhibitors Aspirin Adenosine diphosphate (ADP) receptor

inhibitors Clopidogrel (Plavix) Prasugrel (Effient) Ticagrelor (Brilinta) Ticlopidine (Ticlid) Phosphodiesterase inhibitors Cilostazol (Pletal) Glycoprotein IIB/IIIA inhibitors (intravenous use only) Abciximab (ReoPro) Eptifibatide (Integrilin) Tirofiban (Aggrastat) Adenosine reuptake inhibitors Dipyridamole (Persantine) Thromboxane inhibitors Thromboxane synthase inhibitors Thromboxane receptor antagonists terutroban. Treatment of established arterial thrombosis includes the use of Antiplatelet drugs and thrombolytic therapy. Antiplatelet drugs alter the platelet activation at the site of vascular damage crucial to the development of arterial thrombosis. Aspirin irreversibly inhibits the enzyme COX, resulting in reduced platelet production of TXA2 (thromboxane - powerful vasoconstrictor that lowers cyclic AMP and initiates the platelet release reaction).

Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic AMP with potentiation of the action of PGI2 opposes actions of TXA2 Clopidogrel affects the ADP-dependent activation of IIb/IIIa complex Glycoprotein IIb/IIIa receptor antagonists block a receptor on the platelet for fibrinogen and von Willebrand factor. 3 classes: Murine-human chimeric antibodies (e.g., abciximab) Synthetic peptides (e.g., eptifibatide) Synthetic non-peptides (e.g., tirofiban) Epoprostenol is a prostacyclin that is used to inhibit platelet aggregation during renal dialysis (with or without heparin) and is also used in primary pulmonary hypertension. Thrombolytic therapy is used in myocardial infarction, cerebral infarction, and, on occasion, in massive pulmonary embolism. The main risk is bleeding. Treatment should not be given to patients having had recent bleeding, uncontrolled hypertension or a hemorrhagic stroke, or surgery or other invasive procedures within the previous 10 days. Streptokinase forms a complex with plasminogen, resulting in a conformational change that activates other plasminogen molecules to form plasmin. Plasminogen activators (PA), tissue-type plasminogen activators (alteplase, tenecteplase) are produced by recombinant technology. I. The Cardiac Glycosides (Cardenolides) - the Digitalis Preparations Drug Members : 1. Digitoxin (Crystodigin) 2. Digoxin (Lanoxin) 3. Deslanoside (Cedilanid-D) Quinidine - class Ia drug that prolongs action potential and refractoriness. Procainamide - class Ia drug, has much less effect than quinidine on refractoriness. Disopyramide - a class Ia agent, produces little change in refractory period. Lidocaine - class Ib agent with substantial first-pass hepatic metabolism, is used only parenterally. Mexiletine - class Ib drug, is an analog of lidocaine with similar electrophysiologic actions but has little or no first-pass hepatic metabolism. Tocainide -class Ib, is congener of lidocaine, with little or no first-pass hepatic metabolism.

Phenytoin - class Ib. It was used extensively for arrhythmia management, particularly suppressing the ventricular arrhythmias of digitalis toxicity. Class Ic drugs - are among the most powerful antiarrhythmics but have been associated with a significant risk of proarrhythmia and depression of cardiac contractility. Flecainide - class Ic. By a profound effect on the sodium channel, conduction is markedly slowed but refractoriness is little affected. Encainide - class Ic, has similar efficacy and toxicity to flecainide. Unlike flecainide, encainide has at least 3 active metabolites, which are variably formed depending on genetically inherited degradation pathways.

Coarctation of the aorta Aortic coarctation is a narrowing of part of the aorta (the major artery leading out of the heart). It is a type of birth defect. Coarctation means narrowing. Causes The aorta carries blood from the heart to the vessels that supply the body with blood and nutrients. If part of the aorta is narrowed, it is hard for blood to pass through the artery. Aortic coarctation is more common in persons with certain genetic disorders, such as Turner syndrome. However, it can also be due to birth defects of the aortic valves. Aortic coarctation is one of the more common heart conditions that are present at birth (congenital heart conditions). It is usually diagnosed in children or adults under age 40. Coarctation of the aorta may be seen with other congenital heart defects, such as:

Bicuspid aortic valve Defects in which only one ventricle is present Ventricular septal defect

Symptoms Symptoms depend on how much blood can flow through the artery. Other heart defects may also play a role. Around half of newborns with this problem will have symptoms in the first few days of life. In milder cases, symptoms may not develop until the child has reached adolescence. Symptoms include:

Dizziness or fainting Shortness of breath Pounding headache

Chest pain Cold feet or legs Nosebleed Leg cramps with exercise High blood pressure (hypertension) with exercise Decreased ability to exercise Failure to thrive Poor growth

Note: There may be no symptoms. Managing Coarctation In a critically ill newborn, the goals of management are to improve ventricular function and restore blood flow to the lower body. A continuous intravenous medication, prostaglandin (PGE-1), is used to open the ductus arteriosus (and maintain it in an open state) allowing blood flow to areas beyond the coarctation. It is also often necessary to begin intravenous medications that improve the contraction of the heart. Babies will almost always need to be placed on a ventilator before surgery. In symptomatic newborns with coarctation, surgical repair is usually done on an urgent basis following initial stabilization. Rarely, an infant will not improve with medical therapy and surgery must proceed before the infant has been stabilized. There a number of surgical techniques to repair coarctation. The most common repair involves resection (removal) of the narrowed area with reanastamosis (reconnection) of the two ends to each other. Sometimes the resection (removal) must be extended towards the arch if there is a longer segment of narrowing. Less commonly, the narrowing may be opened with a patch or a portion of an artery may be used as a flap to expand the area (called a subclavian flap aortoplasty). Since older children have less severe symptoms, coarctation repair is typically planned electively. Surgical resection is most commonly performed with resection of the narrowed segment and end-to-end reconnection. Occasionally, patching of the aorta may be necessary.

Tetralogy of Fallot Tetralogy of Fallot refers to a type of congenital heart defect. Congenital means present at birth. Causes Tetralogy of Fallot is classified as a cyanotic heart defect because the condition causes low oxygen levels in the blood. This leads to cyanosis (a bluish-purple color to the skin). Symptoms

Clubbing of fingers (skin or bone enlargement around the fingernails) Cyanosis, which becomes more pronounced when the baby is upset Difficult feeding (poor feeding habits) Failure to gain weight Passing out Poor development Squatting during episodes of cyanosis

Treatment for Tetralogy of Fallot Once tetralogy of Fallot is diagnosed, the immediate management focuses on determining whether the child's oxygen levels are in a safe range. If oxygen levels are critically low soon after birth, a prostaglandin infusion is usually initiated to keep the ductus arteriosus open which will provide additional pulmonary blood flow and increase the child's oxygen level. These infants will usually require surgical intervention in the neonatal period. Infants with normal oxygen levels or only mild cyanosis are usually able to go home in the first week of life. Complete repair is usually done electively when the children are about six months of age, as long as the oxygen levels remain adequate. Progressive or sudden decreases in oxygen saturation may prompt earlier corrective repair. Surgical correction of the defect is always necessary. Occasionally, patients will require a surgical palliative procedure prior to the final correction. Corrective repair of tetralogy of Fallot involves closure of the ventricular septal defect with a synthetic Dacron patch so that the blood can flow normally from the left ventricle to the aorta. The narrowing of the pulmonary valve and right ventricular outflow tract is then augmented (enlarged) by a combination of cutting away (resecting) obstructive muscle tissue in the right ventricle and by enlarging the outflow pathway with a patch. In some babies, however, the coronary arteries will branch across the right ventricular outflow tract where the patch would normally be placed. In these babies an incision in this area to place the patch would damage the coronary artery so this cannot safely be done. When this occurs, a hole is made in the front surface of the right ventricle (avoiding the coronary artery) and a conduit (tube) is sewn from the right ventricle to the bifurcation of the pulmonary arteries to provide unobstructed blood flow from the right ventricle to the lungs.

Transposition of the great vessels

Transposition of the great vessels is a congenital heart defect in which the two major vessels that carry blood away from the heart -- the aorta and the pulmonary artery -- are switched (transposed). Symptoms Blueness of the skin Clubbing of the fingers or toes Poor feeding Shortness of breath Treatment The baby will immediately receive a medicine called prostaglandin through an IV (intravenous line). This medicine helps keep the ductus arteriosus open, allowing some mixing of the two blood circulations. A procedure using cardiac catheterization (balloon atrial septostomy) may be needed to create a large hole in the atrial septum to allow blood to mix. A surgery called an arterial switch procedure is used to permanently correct the problem within the baby's first week of life. This surgery switches the great arteries back to the normal position and keeps the coronary arteries attached to the aorta.