Aortic Stenosis and Regurgitation

Aortic valve stenosis is one of the most prevalent and serious valvular diseases. Calcific degeneration of the aortic valve leaflets is the most common etiology in the US. It is linked to cell death among endothelial cells & fibroblasts and is intricately associated with risk factors akin to atherosclerosis such as hypertension, hyperlipidemia, diabetes mellitus, and inflammation. On histological examination, this degeneration manifests as fine, gritty, white clumps. Furthermore, individuals with bicuspid aortic valves face an increased risk of early dystrophic calcification.

The repercussions of aortic stenosis are far-reaching. Due to the chronically increased afterload, the condition gives rise to concentric hypertrophy of the left ventricle, which paves the way for diastolic heart failure. Additionally, it spurs chronically elevated pressures in the left ventricle and atrium, culminating in LA dilation, hypertrophy, and atrial fibrillation. Clinically, patients present with symptoms akin to heart failure, notably dyspnea on exertion. The heart, under the stress of aortic stenosis, operates under a fixed cardiac output, which not only restricts its ability to surge during stress but also paves the way for symptoms like angina (owing to increased myocardial O2 demand) and syncope (stemming from diminished brain perfusion).

Auscultatory findings reveal a crescendo-decrescendo holosystolic murmur best perceived at the right sternal border, which intensifies upon radiating to the carotid arteries. Severe aortic stenosis presents with a a weak, slow-rising pulse (pulsus parvus et tardus), a later peak in the crescendo, and a muted S2 heart sound. The murmur's intensity can be modulated with specific maneuvers; it amplifies with maneuvers that increase preload (like straight leg raise or squatting) due to augmented stroke volume across the valve. Conversely, maneuvers that decrease preload (like standing or Valsalva) or increase afterload (such as handgrip) decrease murmur intensity due to a reduced stroke volume streaming through the valve. The jet stream through a stenotic aortic valve may also incite hemolytic anemia, which can be detected by the presence of schistocytes on a blood smear.

Aortic regurgitation (AR) is a multifaceted condition that emerges from a myriad of causes. Notably, the valvulitis stemming from acute rheumatic fever can lead to AR, making it the most common causative factor in the developing world. This could further progress to chronic rheumatic heart disease, culminating in aortic stenosis. While Dystrophic calcification is the most common cause of AR in the developed world. Aortic root dilation is also a common etiology, and occurs from a variety of conditions. For instance, aortitis associated with tertiary syphilis, collagen vascular diseases such as Marfan & Ehlers-Danlos syndrome, and ankylosing spondylitis can cause AR due to the dilation of the aortic root. Similarly, large vessel vasculitides like Takayasu arteritis and giant cell arteritis, as well as ankylosing spondylitis, leading to sclerosis of the aortic root, can induce AR. Valve damage from infective endocarditis is another causative agent.

The hemodynamic changes ensuing from AR are profound. AR increases the end diastolic volume and pressure chronically, instigating left ventricular eccentric hypertrophy. This adaptation ensures an increased SV in order to uphold cardiac output. The increased SV in AR manifests as a widened pulse pressure, such as 160/60.

Clinically, AR paints a vivid picture. Its signature sound is a blowing, decrescendo diastolic murmur, best discerned at the left sternal border in the third or fourth intercostal space. Severe instances of AR cause distinct clinical signs: the rapid filling and subsequent collapse of blood vessels, known as the Corrigan pulse, and the characteristic head bobbing with each heartbeat, termed the de Musset sign. The increased pulse pressures in AR can trigger pulsations in the lips or nailbeds known as the Quincke pulse. The dilation accompanying AR in the left ventricle might also elicit an S3 heart sound.