Discussion w9 652

Q-1

Heart Valve Abnormalities – Mitral Valve Regurgitation

Pathology

Mitral regurgitation is a retrograde flow from the left ventricle into the left atrium. Mitral regurgitation leads to left ventricular volume overload due to increased stroke volume, caused by an increase in blood volume within the left atrium and hence an increased preload delivered to the left ventricle during diastole (Douedi, 2021). In chronic progressive MR, ventricular remodeling occurs, allowing maintenance of cardiac output. Over time, there is a positive feedback loop by which volume overload from mitral regurgitation causes ventricular dilatation, widening of the mitral annulus, and diminished coaptation of leaflets, leading to further worsening of mitral regurgitation. Eventually, the volume overload becomes severe that excitation-contraction coupling becomes impaired leading to dilatation and decreased contractility resulting in reduction of ejection fraction (Douedi, 2021).

Etiology

Mitral valve dysfunction may result from irregularities of any portion of the mitral valve apparatus, due to mechanical, traumatic, infectious, degenerative, congenital, or metabolic causes. Mitral valve regurgitation (MR) can be either acute or chronic (Maslow & Poppas, 2017). Typical causes of acute MR include infective endocarditis, ischemic papillary muscle dysfunction or rupture, acute rheumatic fever, and acute dilation of the left ventricle due to myocarditis or ischemia. Common causes of chronic MR include myxomatous degeneration of the mitral leaflets or chordae tendineae, mitral valve prolapse and mitral annular enlargement (Maslow & Poppas, 2017).

Risk Factors

· History of rheumatic heart disease may lead to valvular and sub-valvular fibrosis and leaflet thickening, and various restriction of leaflet motion.

· Infective endocarditis causes mitral regurgitation to develop associated vegetations that are echocardiographic hallmarks of the disease. In infective endocarditis there is leaflet or chordal disruption, perforations and flail.

· Mitral valve prolapse can result from abnormal elasticity which includes redundancy and enlargement of various parts of the mitral valvular apparatus such as the chordae tendinae, leaflets and mitral annulus.

· History of ischemic heart disease the left ventricle undergoes enlargement and remodelling which leads to mitral regurgitation caused by apical tethering of normal leaflets (Maslow & Poppas, 2017).

Signs and Symptoms

The common presenting symptoms of mitral regurgitation are holosystolic blowing murmur at the apex that commonly radiates to the axilla, dyspnea on exertion, decreased exercise tolerance and lower extremity edema. Other factors to include fatigue and displaced point of maximal impulse which indicates severe and chronic mitral regurgitation (Maslow & Poppas, 2017).

Diagnostics

Transthoracic echocardiogram is the definitive test in determining the right ventricular systolic pressure, severity, mechanism, presence of flail, measuring the left ventricular size and function, left atrial size, and other valvular abnormalities. It is also useful for assessing serial changes in left ventricular size and function, and evaluating the patient after a change in symptoms. Spatial mapping, flow convergence, pulmonary vein velocity patterns, vena contracta width, continuous-wave Doppler density and shape, and quantification of antegrade valvular flow volumes can be used to further assess severity (Maslow & Poppas, 2017). Transesophageal echocardiogram may be needed to better assess the severity and etiology in rare occasions where the degree of symptoms does not match transthoracic echocardiogram findings. A stress echocardiogram is often useful for determining the severity and impact of the disease on the patient's exercise hemodynamics. All patients must undergo ECG exam as a routine screening as well as for any rhythm disturbance such as atrial fibrillation (Maslow & Poppas, 2017).

Treatments

Acute mitral regurgitation is a medical emergency and surgery is indicated. Prior to surgery, afterload reduction is necessary such as ordering diuretics to stabilize the patient. Furosemide 20-200 mg orally once to twice daily is usually given (Douedi, 2021). Intra-aortic balloon counter pulsation is indicated for severe acute mitral regurgitation associated with hypotension. There is no accepted medical treatment for asymptomatic patients with preserved left ventricular function; however, these patients are closely monitored for risk factors such as hypertension. Asymptomatic patients with impaired left ventricular function are usually treated with angiotensin-converting enzyme (ACE) inhibitors and beta-blockers. Indications for surgery include depressed left ventricular function and elevated left atrial pressures (Douedi, 2021). For asymptomatic patients, surgery is indicated if they have a depressed left ventricular ejection fraction of 60% or less and/or left ventricular end-systolic diameter of 45 mm or more. In chronic symptomatic mitral regurgitation, all patients should be treated with ACE inhibitors, beta-blockers, and diuretics. Once the patient is stabilized, the treatment of choice is surgery, indicated for all patients with New York Heart Association class II, III, and IV symptoms (Douedi, 2021).

References:

Douedi, S. (2021, March 10). Mitral regurgitation. Retrieved May 03, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK553135/

Maslow, A. D., & Poppas, A. (2017). Primary mitral valve regurgitation: Update and review. Global Cardiology Science and Practice, 2017(1). doi:10.21542/gcsp.2017.3

Q-2

Aortic Stenosis

Aortic stenosis (AS) is the narrowing of the aortic valve reducing blood flow to the body. Most cases of aortic stenosis can be due to congenital valvular disease, degenerative calcification, and rheumatic heart disease. Calcification of the valve is associated with aortic stenosis (AS) due to chronic inflammation, which is the result of an increase in age and modifiable risk factors including hypertension, hyperlipidemia, diabetes, and smoking (Paul & Das, 2017). Patients may report syncope, angina chest pain during physical activity, and paroxysmal nocturnal dyspnea, which are the classic triad symptoms of AS. Upon auscultation, paradoxical splitting of the S2, ejection clicks, and a systolic murmur can be demonstrated. The murmur can be augmented when the patient is squatting as this increases stroke volume. In severe AS, the carotid pulse can be slow-rising, late-peaking and low-amplitude, and there may be a lag between the apical impulse and the carotid impulse (Jelavic & Pintaric, 2019). Additionally, the systolic pressure would be elevated with AS.

A transthoracic echocardiogram (TTE) is primarily utilized for valvular heart disease and can confirm the diagnosis as it reveals the structure and functions of the heart valves, left ventricular hypertrophy, and LV function (Jelavic & Pintaric, 2019). Additionally, echocardiography can evaluate valve obstruction and LV outflows, such as mean gradient and aortic valve area, to determine the grading of mild, moderate, and severe obstruction. Additionally, a CT scan would be essential in cases with suspected aortic root disease, especially for patients with a congenital bicuspid valve (Paul & Das, 2017). It is also necessary for clinical decision-making and surgical planning. Cardiac catheterization is also utilized for accurate measurement of AS and hemodynamic assessment, such as LV end-diastolic and systolic volume and ejection fraction.

Although no medications can treat valve problems of AS, medications can help reduce the effects. Patients with mild to moderate AS may be prescribed ACE inhibitors for hypertension, antiarrhythmics such as a beta-blocker, and a diuretic to prevent fluid overload (Jelavic & Pintaric, 2019). Additionally, patients should be encouraged to healthier eating habits, increase exercise, smoke cessation, and better manage stress. However, progressive AS leads to left ventricular dysfunction and an increase in myocardial oxygen demand, and mortality increases in symptomatic patients with an overall age of two to three-year survival rates (Jelavic & Pintaric, 2019). Therefore, patients with severe AS will need an aortic valve replacement as it is the only effective treatment for hemodynamic instability.

 

References

Jelavic, M., & Pintaric, H. (2019). Aortic stenosis from the perspective of the current guidelines. Medical Sciences, 537, 46-47. https://doi.org/10.21857/yq32oh40d9

Paul, A., & Das, S. (2017). Valvular heart disease and anaesthesia. Indian Journal of Anaesthesia, 61(9), 721–727. https://doi.org/10.4103/ija.IJA_378_17

Q-3

Ischemic cardiomyopathy

Pathology/etiology

Ischemic cardiomyopathy (ICM) occurs due to ischemic damage to the myocardium that results in a number of clinical changes and commonly leads to heart failure. A major precursor of ICM is progressive coronary artery disease and a history of myocardial infarctions.is which eventually leads to ischemia that results in irreversible cardiac muscle damage and cardiac remodeling. Histologic examination of the myocardium typically shows nonspecific changes of fibrosis and hypertrophy. It also reveals myocardial injury with infiltrates by inflammatory cells. Furthermore, there is a significant impairment of the left ventricular systolic function, with a left ventricular ejection fraction of less than 40 percent (Briceno, Schuster, Lumley, & Perera, 2016).

Presentation

Signs and symptoms may vary between patients and their degree of physiological compensation. Some patient may be asymptomatic or present with mild anginal chest pain and dyspnea on exertion whereas some patients may present with overt heart failure symptoms which include dyspnea, orthopnea, poor exercise tolerance, and increased fatigability. Physical evaluation often includes bilateral lower extremity edema, bibasilar crackles, S3 gallop, displaced PMI, carotid bruits, JVD, and hepato-jugular reflex (Briceno et al., 2016).

Risk factors

Modifiable risk factors include diabetes mellitus, hypertension, tobacco abuse, hyperlipidemia, obesity, and a sedentary lifestyle. Non-modifiable risk factors include age, gender, and genetics (Briceno et al., 2016).

Diagnostics

In addition to a history and physical exam, BMP, a chest x-ray, and transthoracic echocardiography (TTE) are useful in the diagnosis of ICM. A stress test is also beneficial for assessing for cardiac ischemia. Coronary angiography allows for direct visualization of the coronary arteries, level of obstruction, and the blood flow to the myocardium and can be used for percutaneous coronary intervention with balloon angioplasty and coronary stents to allow for better blood flow across occluded coronary artery (Sisakian, 2016).

Treatment

Management of ICM involves goal-directed medical therapy targeting the underlying cause and reversal of myocardial remodeling. Patients primarily benefit from lifestyle modifications that include smoking cessation, diet changes, and exercise. Pharmacological management includes aspirin, spironolactone, a high potency statin, ACE inhibitors, an ARNI like valsartan/sacubitril, and sodium current inhibitors such as ranolazine, which has antiischemic/antianginal properties. Many patients also benefit from coronary revascularisation, including coronary angioplasty or coronary artery bypass grafting. Patients with an EF of 30 percent and associated HF with NYHA functional class II or III are considered for ICD placement and resynchronization therapy as primary prevention of sudden cardiac death (Sisakian, 2016).

 

Briceno, N., Schuster, A., Lumley, M., & Perera, D. (2016). Ischaemic cardiomyopathy: pathophysiology, assessment and the role of . Heart (British Cardiac Society), 102(5), 397–406. https://doi.org/10.1136/heartjnl-2015-308037

Sisakian H. (2016). Cardiomyopathies: Evolution of pathogenesis concepts and potential for new therapies. World journal of cardiology, 6(6), 478–494. https://doi.org/10.4330/wjc.v6.i6.47