Case 1: Management of Patent Foramen Ovale
A 26-year-old woman presented to the emergency department (ED) with chest pain for 1 day. The chest pain started suddenly, was nonradiating, and was associated with arm movement. She did house cleaning 1 day prior to presentation. The pain was not relieved by taking over-the-counter medication. She denied palpitations, dizziness, shortness of breath, and trauma. Her family history and social history were unremarkable. On presentation to the ED, her vital signs were stable. On physical examination, she did not have any significant findings except chest wall tenderness. Her ECG showed first-degree atrioventricular block. Initial laboratory findings were unremarkable. She was given analgesics. The patient was transferred to the telemetry floor, where an echocardiogram was performed, which showed a normal left ventricular ejection fraction with no wall motion or valvular abnormality and a small patent foramen ovale (PFO). How would you manage this case?
This patient is a young asymptomatic woman who presented with musculoskeletal chest pain. Incidentally, she was noted to have a PFO, which is asymptomatic and does not require any treatment.
PFO is an opening in the atrial wall at the location of the fossa ovalis that remains open beyond 1 year of life. After birth, when the pulmonary circulation develops, the foramen ovale closes due to the increase in left atrial pressures, which takes up to 1 year.
PFO is usually asymptomatic and is often found incidentally. However, it carries a risk of paradoxical embolism in high-risk patients. Some patients present with systemic embolism causing organ infarcts and even myocardial infarction.
The diagnostic test of choice is echocardiography. PFO can be detected using color flow Doppler, contrast echocardiography, and transmitral Doppler.
Isolated PFO does not usually require any treatment unless it is associated with an unexplained neurologic event. Such conditions are treated with antiplatelet drugs and anticoagulation therapy. Percutaneous closure of the PFO is an option when there is contraindication to medical management and anticoagulant treatment, in the setting of paradoxical embolism or cryptogenic stroke. Surgical closure is indicated when the opening is >25 mm or when there is failure of a percutaneous device.
PFO is usually asymptomatic and is often found incidentally.
Isolated PFO does not usually require any treatment unless it is associated with an unexplained neurologic event.
Case 2: Management of Aortic Stenosis
A 78-year-old man with a medical history of hypertension and chronic obstructive pulmonary disease presented to the emergency department with worsening exercise tolerance for the past 6 months. He usually walks to his workplace, which is 6 blocks away from his home, but for the past few months, he has been barely able to walk for 2 to 3 blocks and has had to stop every 10 to 15 minutes to rest due to shortness of breath and chest tightness. On examination, the patient had a regular pulse and a blood pressure of 100/63 mm Hg and was afebrile. Examination revealed a thin body habitus. Cardiovascular examination revealed a hyperdynamic apical beat, systolic murmur in the aortic area, and carotid bruits. ECG showed normal sinus rhythm with left ventricular hypertrophy pattern. How would you manage this case?
This case describes an elderly man with gradual worsening of cardiac symptoms. Examination is significant for wide pulse pressure and a systolic murmur best heard in the aortic area. ECG shows left ventricular hypertrophy (LVH). These factors point toward aortic stenosis (AS) as the most likely diagnosis in this patient. The etiology in this case is most likely calcification of the aortic valves. There are various manifestations of AS, which are described later in detail. Management includes both pharmacologic and surgical treatments depending on the degree of stenosis.
AS is common in the elderly population. Etiology includes congenital valve abnormalities, calcification of the valve, trauma to the valve, and rheumatic heart disease, among other causes. The normal aortic valve area is approximately 3 to 4 cm2 in adults. Usually patients are asymptomatic in their early stages. As the stenosis progresses, symptoms become more prominent, and the patient classically presents with syncope, angina, and heart failure. Physical examination findings are often clues to the diagnosis, including single S2 on auscultation and a systolic ejection murmur with radiation to carotid vessels.
Symptoms include dyspnea on exertion, dizziness, decreased exercise tolerance, syncope, chest pain or exertional angina, and palpitations.
Echocardiogram is used to diagnose and evaluate the severity of AS. ECG usually shows LVH but is not diagnostic for AS. Doppler echocardiography can be used to assess the transaortic velocity, the left ventricular-aortic gradient, and the valve area.
There are various stages of severity of AS depending on the transvalvular aortic velocity. These include the following:
Stage A: Includes maximum transvalvular aortic velocity <2 m/s. These patients are usually asymptomatic and have congenital aortic valve anomaly or aortic sclerosis or other risk factors for aortic valve disease such as smoking, male sex, metabolic syndrome, or old age.
Stage B: Includes mild to moderate AS. These patients are usually symptomatic. The transvalvular aortic velocity for mild AS is 2.0 to 2.9 m/s, or the mean transvalvular pressure gradient is <20 mm Hg. For moderate AS, the transvalvular aortic velocity is 3.0 to 3.9 m/s, or the mean transvalvular pressure gradient is 20 to 39 mm Hg.
Stage C: Includes severe valve obstruction but patients are asymptomatic. There is reduced leaflet motion and transvalvular aortic velocity ≥4 m/s. The aortic valve area is ≤1.0 cm2.
Stage D: Includes symptomatic patients with severe AS.
Treatment is usually valve replacement in patients who have severe AS. Balloon valvuloplasty is indicated in patients for palliative purposes. Pharmacologic management can be used in reducing symptoms but requires caution because even a mild imbalance can lead to hemodynamic instability. Diuretics, angiotensin-converting enzyme inhibitors, β-blockers, and sometimes digitalis can be used.
AS commonly presents with syncope, angina, or heart failure.
Classification of AS is important because management varies based on stage.
Definitive treatment includes aortic valve replacement.
Case 3: Management of Mitral Stenosis
A 37-year-old woman was admitted to the telemetry floor for shortness of breath for 3 days. She immigrated from India recently and had a medical history significant for tuberculosis in childhood (completed treatment) and left chronic otitis media since childhood. She denied cough, fever, weight loss, or dizziness. She has 2 children and had no complications during pregnancy or in the postpartum period. The patient had stable vital signs. On examination, she was found to have a grade 2/6 mid-diastolic murmur in the mitral area worsened by expiration and heard best in the left lateral position. The rest of the examination was normal. ECG showed normal sinus rhythm with bifid P waves. Pro-B-type natriuretic peptide was elevated. She was started on furosemide, and echocardiography was planned. How would you manage this patient?
There are various causes of diastolic murmur in the mitral area. The murmur is typical for mitral stenosis (MS). This is a young patient with recurrent upper respiratory infection in childhood, who recently immigrated from a developing country and presented with a diastolic murmur in the mitral area. Childhood- or adult-onset rheumatic heart disease should be considered in this patient. MS can congenital or due to acquired calcification of the mitral valve. Most cases are secondary to rheumatic heart disease causing adhesions, thickening, and fibrosis of mitral leaflets, leading to MS. In this scenario, the patient appears to have congestive symptoms due to MS and will need further evaluation to assess the severity and determine further management.
MS can be congenital or acquired, but most cases are attributed to rheumatic heart disease. The progression can be slow, but some patients can progress rapidly to heart failure, especially during pregnancy or when they have other significant comorbidities. The symptoms usually depend on the severity of stenosis.
Patients with MS are at a risk of developing atrial fibrillation secondary to atrial dilatation. This occurs due to increase in left atrial pressure due to mitral stenosis causing left atrial enlargement. This in turn causes stagnation of blood, leading to clot formation and the risk of thromboembolism. In addition, atrial fibrillation causes loss of atrial contraction, which is necessary for forward movement of blood, especially in patients with MS. Because these patients have a deformed mitral valve, it puts them at high risk for infective endocarditis.
MS can present with decreased exercise tolerance, dyspnea, orthopnea, fatigue, chest pain, palpitations (if atrial fibrillation develops), stroke (secondary to thromboembolism), hemoptysis (due to pulmonary vascular congestion), hoarseness (also known as Ortner syndrome and caused by compression of the recurrent laryngeal nerve by the enlarged left atrium), and even signs of right heart failure such as jugular venous distension, tender hepatomegaly, ascites, and pedal edema. Most of these symptoms are due to the backpressure caused by a narrowed mitral orifice, ultimately leading to pulmonary hypertension, increased right ventricular enlargement, tricuspid regurgitation, right atrial enlargement, and ultimately right heart failure.
On examination, MS patients can have diminished pulse volume. An irregularly irregular pulse will be present if the patient develops atrial fibrillation. Auscultation of the heart will reveal a loud S1, but as the valves calcify, the S1 diminishes in intensity. An opening snap is characteristic but may not be present in all cases. MS murmur is typically a low-pitched mid-diastolic murmur that is most prominent at the apex. Patients with pulmonary edema can have rales on lung examination. Signs of right-sided heart failure includes jugular venous distention, tender hepatomegaly, and pedal edema.
Echocardiogram is diagnostic for MS. The degree of stenosis is essential for management. Pharmacologic management has limited role in mitral stenosis. β-Blockers and diuretics can be used with caution. Patients with atrial fibrillation will benefit from rate control medications and anticoagulation therapy.
MS is classified into various stages as shown in the table below.
|Stage A||Risk of MS||None||None|
|Stage B||Progressive MS||Increased transmitral flow velocities Mitral valve area (MVA) >1.5 cm2||None|
|Stage C||Asymptomatic, severe MS||MVA ≤1.5 cm2 (MVA ≤1 cm2 with severe MS)||None|
|Stage D||Symptomatic severe MS||MVA ≤1.5 cm2 (MVA ≤1 cm2 with severe MS)||Yes|
Surgery is recommended for patients with stage D MS. Options include balloon valvuloplasty and commissurotomy.
MS is most commonly caused by rheumatic heart disease.
The murmur typically present is a mid-diastolic murmur most prominent in the apex.
There is limited role for pharmacologic management in MS.
For patients with severe MS with symptoms, surgical therapy is warranted.
Case 4: Management of Mitral Regurgitation
A 56-year-old man was admitted to the hospital with shortness of breath for 1 day. He was not able to lay flat and was feeling tired even while doing minimal activities. He recently experienced an anterior wall myocardial infarction (MI) for which he underwent percutaneous coronary intervention with stent placement and was discharged 2 days ago with medications. Prior to the MI, the patient was completely asymptomatic, and he has been compliant with medications. At presentation, the vital signs were stable. On physical examination, pulse was regular. Cardiac examination revealed a systolic murmur that was more prominent in the apex, radiating to the axilla. Lung examination showed bilateral crackles. ECG showed normal sinus rhythm with Q waves in inferior leads. Pro-B-type natriuretic peptide was elevated. He was planned for echocardiography. How would you manage this case?
This patient has a systolic murmur in the apex radiating to axilla. Most likely, this patient developed acute mitral regurgitation (MR) after MI, which is a complication of MI. Such patients usually present with symptoms such as dyspnea, orthopnea, decreased exercise tolerance, and fatigue. In this case, the patient will need medications to reduce afterload to minimize symptoms due to MR. Diuretics can also be used for symptomatic relief. Surgical intervention is required in follow-up care.
Acute MR is a common complication of MI. Other causes of MR include rheumatic heart disease, mitral valve prolapse, ischemic heart diseases, cardiomyopathy, infective endocarditis, and annular calcification. These patients are usually symptomatic due to the acute onset. Symptoms are partly due to impaired left ventricular (LV) function. The murmur is typically described as a high-pitched, blowing, holosystolic murmur best heard at the apex and radiating to axilla. S1 may be diminished, S2 is split, and a loud S3 may be present. Mild MR is usually asymptomatic, but as the MR progresses in severity, LV failure occurs, causing pulmonary edema and, in turn, right heart failure.