A patient has dyspnea, syncope and angina. What is the most likely diagnosis?
Ans. a. Aortic stenosis (Ref: Harrison 19/e p1529. 18/e p 1939)Patients of aortic stenosis have dyspnea, syncope and angina.'Most patients with pure or predominant AS have gradually increasing obstruction over years, but do not become symptomatic until the sixth to eighth decades. Exertional dyspnea, angina pectoris, and syncope are the three cardinal symptoms. Often, there is a history of insidious progression of fatigue and dyspnea associated with gradual curtailment of activities. Dyspnea results primarily from elevation of the pulmonary capillary pressure caused by elevations of LV diastolic pressures secondary to reduced left ventricular compliance and impaired relaxation. Angina pectoris usually develops somewhat later and reflects an imbalance between the augmented myocardial oxygen requirements and reduced oxygen availability.: Exertional syncope may result from a decline in arterial pressure caused by vasodilation in the exercising muscles and inadequate vasoconstriction in non-exercising muscles in the face of a fixed CO, or from a sudden fall in CO produced by an arrhythmia. '- Harrison 18/e p1939Aortic stenosisEtiology:Congenital (bicuspid, unicuspid). Degenerative calcific. Rheumatic fever. RadiationSymptoms:AS is rarely of clinical importance until the valve orifice has narrowed to approximately 1 cm2.Once symptoms occur, valve replacement is indicatedQ.Most patients with pure or predominant AS have gradually increasingQ obstruction over years, but do not become symptomatic until the sixth to eighth decadesQ.Exertional dyspnea, angina pectoris, and syncope are the three cardinal symptomsQ.Often, there is a history of insidious progression of fatigue and dyspnea associated with gradual curtailment of activitiesQ.Because the CO at rest is usually well maintained until late in the course, marked fatigability, weakness, peripheral cyanosis, cachexia, and other clinical manifestations of a low CO are usually not prominent until this stage is reachedQ.Orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema, i.e., symptoms of LV failure, also occur only in the advanced stages of the diseaseQ.Severe pulmonary hypertension leading to RV failure and systemic venous hypertension, hepatomegaly, AF, and TR are usually late findings in patients with isolated severe ASQ.Death in patients with severe AS occurs most commonly in the 7th and 8th decadesQ.Auscultation:An early systolic ejection sound is frequently audible in children, adolescents, and young adults with congenital BAV diseaseQ.Paradoxical splitting of S2QS4: Audible at the apexQS3 generally occurs late in the courseQEjection (mid) systolic murmurQEjection (mid) systolic murmur in AS* Commences shortly after the S1* Increases in intensity to reach a peak toward the middle of ejectionQ* Ends just before aortic valve closureQ* Characteristically low-pitched, rough and rasping in character, and loudest at the base of the heart, most commonly in the 2nd right intercostal spaceQ.* Transmitted upward along the carotid arteries* Occasionally, transmitted downward and to the apex, where it may be confused with the systolic murmur of MR (Gallavardin effectQ).Echocardiography:The key findings on TTE are thickening, calcification, and reduced systolic opening of the valve leaflets and LV hypertrophyQ.Eccentric closure of the aortic valve cusps is characteristic of congenitally bicuspid valvesQ.Severity of ASValve AreaMild1.5-2 cm2Moderate1-1.5 cm2Severe<1 cm2Echocardiography is useful for identifying coexisting valvular abnormalities: for differentiating valvular AS from other forms of LV outflow obstruction: and for measurement of the aortic root and proximal ascending aortic dimensionQ.Dobutamine stress echocardiography is useful for the evaluation of patients with AS and severe LV systolic dysfunction (EF < 0.35), in whom the severity of the AS can often be difficult to judge.
Aortic stenosis
Aortic regurgitation
Atrial septal defect
Ventricular septal defect
C.V.S.