Question

A 33 year old woman reporting exertional chest pain undergoes a Doppler echocardiogram, which shows concentric thickening of the left ventricle, thickened aortic valve leaflets and a 67 mmHg pressure gradient from the left ventricle to the aortic root.

1) Why does this patient have chest pain upon exertion?

2) Would you expect there to be a change in this patient’s EF and CO?

3) What is the ling term prognosis for this patient in terms of cardiac function?

Answer 1

1) Why does this patient have chest pain upon exertion:

Valves sclerosis is thickening of the valve without any significant effect on the function of the valve itself. Heart valve stenosis is thickening and tightening of the valve that leads to the heart having to work harder and the possibility of not enough blood being delivered to the body. The risk of aortic sclerosis progressing to aortic stenosis is low. The rate of progression to clinical aortic stenosis is under 2% per year this may lead severe chest pain.

change in this patient’s Ejection fraction

Despite its significant impact on intermediate all-cause mortality at univariate analysis (log-rank test: P = 0.045, Fig. , atherosclerosis of the ascending aorta was not predictive of intermediate all-cause mortality at multivariate analysis. Cox regression analysis showed that ascending aortic wall thickness was a significant predictor of all-cause mortality along with patient's age, serum creatinine, left ventricular ejection fraction ≤50% and emergency surgery . These findings did not change when gender was included in the regression model. Similar findings were also observed when aortic wall thickness was included in the regression model as quintiles [P < 0.0001; relative risk (RR): 1.628; 95% confidence interval (CI): 1.219–1.2.176; Fig. 2]. Since Kaplan–Meier analysis showed that the mortality risk according to quintiles of aortic wall thickness (log-rank test: P = 0.004) was markedly increased when aortic wall thickness was ≥1.8 mm (5-year freedom from any fatal event: 82.2 vs. 92.6%, P < 0.0001), this cut-off value was considered for further analysis. Cox regression analysis showed that aortic wall thickness ≥1.8 mm was an independent risk factor for intermediate all-cause mortality (P = 0.001; RR: 2.356; 95% CI: 1.427–3.889;

Cardiac Out Put:

When the mitral valve area goes below 2 cm², the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood increases. Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion.^{[citation needed]}

When the mitral valve area goes less than 1 cm², there will be an increase in the left atrial pressures (required to push blood through the stenotic valve). Since the normal left ventricular diastolic pressures is about 5 mmHg, a pressure gradient across the mitral valve of 20 mmHg due to severe mitral stenosis will cause a left atrial pressure of about 25 mmHg. This left atrial pressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension. Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and pooling of fluid in the lungs (congestive heart failure causing pulmonary edema).^{[citation needed]}

The constant pressure overload of the left atrium will cause the left atrium to increase in size. As the left atrium increases in size, it becomes more prone to develop atrial fibrillation (AF). When atrial fibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction).^{[citation needed]}

In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick. The loss of the atrial kick due to atrial fibrillation ( i.e. blood cannot flow into the left ventricle thus accumulating in the left atrium ) can cause a precipitous decrease in cardiac output and sudden congestive heart failure

Progonosis:

progressive increase in LV dimensions or a decline in resting ejection fraction during serial follow-up may identify high-risk patients who require careful monitoring. Patients with even moderate symptoms or evidence of severe LV dilatation are at higher risk and should be considered for early intervention. These findings emphasize the importance of close follow-up of patients with chronic AR, including those who are asymptomatic