Revascularization via percutaneous coronary intervention (PCI) is often indicated for patients who fail medical therapy or do not tolerate medical therapy. For patients who do not have symptom control with medical therapy, PCI often improves symptoms.⁹ Other interventions such as coronary artery bypass grafting (CABG) may also be indicated depending on the severity and location of coronary lesions; however, such guidelines are beyond the scope of this book.

Vasospastic angina is an alternative condition, which is a result of vasospasm in patients who may or may not have obstructive coronary lesions. It clinically presents with rest angina associated with ST elevation or ST depression on ECG, and pain typically promptly responds to sublingual nitrates. Diagnosis has three components: nitrate responsiveness, transient ischemic ECG changes with no obvious cause, and angiographic evidence of coronary artery spasm. Risk factors and triggers include certain drugs such as cocaine.

Chronic treatment focuses on prevention of recurrence and typically includes the use of calcium channel blockers. Long-acting nitrates are second line for chronic treatment. Nonselective beta-blockers should be avoided due to the possibility of unopposed alpha stimulation of the coronary vessels.²⁰

The pericardium is a fibroelastic sac that surrounds the heart composed of two layers: an outer fibrous layer and an inner serous layer. Pericardial fluid is contained between these two layers.

Acute pericarditis is the result of inflammation of the pericardial sac. Patients with acute pericarditis tend to present with chest pain of sudden onset that can be described as sharp and pleuritic (worsened with cough or inspiration), and it improves with sitting up and leaning forward. Sitting up and leaning forward relieves pain via a reduction of pressure on the parietal pericardium. Pain associated with this condition may also radiate to the trapezius ridge. Radiation of pain is due to referred pain.²¹

In developed countries, the most common cause is presumed to be viral in origin, and pericarditis often follows a flulike or gastrointestinal syndrome. In developing countries, tuberculosis is the most common cause. Other causes include autoimmune diseases such as systemic lupus erythematosus, hypothyroidism, radiation, cancer, and postcardiac injury syndrome, which can manifest after procedures such as PCI, pacemaker insertion, or transcatheter aortic valve replacement. However, often a cause is not found, and most cases are classified as idiopathic.

Diagnosis involves a combination of history, physical examination, laboratory, and imaging studies. History involves chest pain with characteristics described above. On physical examination, patients may have a pericardial friction rub that can be heard with the patient leaning forward as a result of friction caused by inflammation between the layers of the pericardium. ECG findings classically show diffuse ST elevation and PR depression.

Should patients have involvement of the myocardium, troponin may be elevated but does not indicate prognosis in these patients.²² If there is severe involvement of the myocardium, LV wall motion may be severely depressed. Inflammatory markers, such as ESR, and CRP are elevated in most cases but are not specific for this condition. Studies have shown, however, that high-sensitivity CRP identifies patients who have a higher risk of recurrence.²³

Imaging also aids in diagnosis, and often echocardiography is all that is needed. Imaging can help identify complications such as tamponade and constrictive pericarditis as well as to identify and quantify any associated pericardial effusion. It can also be used to assess myocardial function in the setting of possible myocardial involvement.²⁴

Anti-inflammatory medication is the primary treatment for acute pericarditis and its associated pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the first-line treatment in these patients. Options include ibuprofen, indomethacin, and ketorolac (if patients cannot take oral medications). If patients have concomitant coronary artery disease, aspirin is preferred to NSAIDs. Colchicine, a microtubule inhibitor, should also be added as it has been shown to reduce “incessant and recurrent pericarditis.”²⁵ Steroids have been used as second- or third-line treatments, with low-dose steroids being superior to high-dose steroids, with lowdose steroids having a lower rate of treatment failure and recurrence.²⁶ Trials investigating other anti-inflammatory agents, such as IL-1 inhibitors, are underway.

Invasive interventions are indicated for patients who develop tamponade or constrictive pericarditis. In the case of cardiac tamponade, pericardiocentesis or a surgical pericardial window is indicated. Should a patient have constrictive pericarditis with active inflammation, anti-inflammatory therapy is attempted first, and pericardiectomy is performed in refractory cases. Should constrictive pericarditis be present without active inflammation, pericardiectomy is the first-line treatment.

Aortic dissection is a rare clinical condition that presents acutely with severe chest or back pain and acute hemodynamic instability. Most commonly, aortic dissections result from an intimal tear leading to a “dissection” of blood that courses along the tunica media and separates the tissues along its course. Dissections can course as far as the iliac arteries or even further.

There are various complications associated with aortic dissection, which may include rupture into the pericardium leading to tamponade, acute dissection of the aortic valvular annulus leading to acute aortic regurgitation, dissection extension into the coronary arteries leading to myocardial infarction, and renal or other end-organ failure due to obstruction of branches such as the renal arteries or carotid arteries.

There are two anatomical classifications to aortic dissection, the Debakey and Stanford classifications, but the Stanford (Daily) system is more widely used. Dissections involving the ascending aorta are classified as type A dissections, while those that involve sites distal to the ascending aorta are classified as type B dissections.

Risk factors for aortic dissection include hypertension (the most important factor), cocaine use (leads to an abrupt change in blood pressure), connective tissue disorders such as Marfan or Ehlers-Danlos syndromes, preexisting aortic aneurysm, bicuspid aortic valve, aortic instrumentation or surgery, coarctation of the aorta, Turner syndrome, and vasculitides such as Takayasu and giant cell arteritis.²⁷,²⁸

Patients with acute aortic dissection can have variable symptoms depending on the extent of dissection and the structures affected. Pain associated with this condition is most commonly abrupt, knifelike, and is located in the chest or back. Patients describe this as pain they have never experienced before. Type A dissections tend to be associated with more pain in the anterior chest, while type B dissections tend to be associated with more pain in the back. Pain can radiate anywhere in the thorax or the abdomen. Syncope, heart failure, or stroke may be other presenting symptoms, though painless dissection is relatively uncommon.

Other symptoms that may be noted include pulse differential between extremities due to extension to the subclavian artery in some cases. In addition, lower extremity pulses may be affected if the dissection extends to the iliac vessels. Patients may also have focal neurological deficits as well as acute aortic valve regurgitation.

Diagnosis of aortic dissection is often a combination of history, physical examination, and imaging studies. CT angiography is the most common imaging study used for diagnosis if the patient is hemodynamically stable, but TEE can also be used. In fact, TEE is typically recommended for diagnosis if the patient is hemodynamically unstable, as this suggests involvement of the ascending aorta.²⁹

Management varies depending if the patient has a type A or type B aortic dissection. In general, type A dissections require emergent surgery, whereas type B should be medically managed. Early management focuses on pain control and limiting propagation of the dissection via “impulse control” therapy. Typically, this involves controlling blood pressure by keeping systolic blood pressure between 100 and 120 mm Hg and heart rate <60 beats per minute. Common medications used for this purpose include esmolol or labetalol as well as vasodilators such as nitroprusside or nicardipine. Care must be taken that vasodilators are not begun until after beta-blockade is established, as vasodilators can lead to a reflex tachycardia. In terms of pain control, IV opioids are preferred.³⁰

As stated above, a type A aortic dissection is a surgical emergency. A type B dissection that shows evidence of malperfusion is treated with aortic stent-grafting or surgery, but a type B dissection without malperfusion can be managed medically with impulse control and serial imaging.

A median sternotomy is the most common incision for open heart surgeries, as it affords the best access to the mediastinum and provides for easier exposure of every chamber and valve of the heart, with the exception of the posterior-lying left atrium.³¹ A median sternotomy involves a longitudinal incision through the sternum, which is composed of three parts: the manubrium, body, and xiphoid process. In broad terms, the anterior thoracic wall is innervated by the intercostal nerves, which are formed by the anterior rami of the T1-T11 spinal nerves.³² After exiting the intervertebral foramina, these nerves travel anteriorly in between the innermost and internal intercostal muscles. As they pass the internal mammary artery, they rise anteriorly and become the anterior cutaneous branch of the intercostal nerves.³ More specifically, the anterior thoracic wall is innervated by the anterior cutaneous branches of the 2nd-6th intercostal nerves, while the posterior and lateral walls are innervated by the 2nd-11th intercostal nerves. Each thoracic nerve provides innervation to a striplike dermatome of the chest wall, with the exception of T1, which typically supplies only a small portion of the back and most of the medial forearm.³² The area overlying the manubrium and superior-most aspects of the sternal body is innervated by the supraclavicular nerve, which arises from the C3 and C4 nerve roots. A dermatomal map is illustrated in Figure 13.1.