Chest pain is a frequently reported and often alarming symptom of a COVID-19 infection, ranging from a mild ache to a severe sensation. This discomfort arises from several distinct biological and mechanical processes, making it a complex symptom to evaluate. The primary mechanisms involve widespread inflammation, direct viral interaction with the cardiovascular system, and the body’s tendency to form blood clots.
Inflammatory Effects in the Lungs and Lining
The respiratory system is a primary target of the SARS-CoV-2 virus, and the resulting immune response causes significant inflammation that manifests as chest pain. A specific cause is pleurisy, which involves the inflammation of the pleura, the thin layers of tissue surrounding the lungs and lining the chest cavity. When these layers become inflamed, they rub against each other instead of gliding smoothly during breathing, causing pain.
Pleurisy typically causes a sharp, stabbing pain that worsens when a person takes a deep breath, coughs, or moves their torso. This is known as pleuritic chest pain, directly linked to the mechanics of respiration. Beyond the lining, the extensive inflammation associated with COVID-19 pneumonia can cause a more generalized chest discomfort. When the virus infects the lung tissue itself, the resulting inflammatory response can make the chest feel heavy or tight.
Direct Heart Involvement
The virus can directly or indirectly affect the cardiovascular system, leading to inflammatory conditions of the heart that cause chest pain. Myocarditis is the inflammation of the heart muscle (myocardium). Damage to the heart muscle can be caused by the virus itself or by the body’s overactive immune response, often involving a massive release of inflammatory signaling molecules known as a cytokine storm.
Pericarditis is the inflammation of the pericardium, the fluid-filled sac that encases the heart. The pain is often described as a sharp, central chest pain or pressure. A characteristic feature is that the pain is often alleviated by sitting up and leaning forward, and it may worsen when lying down or taking a deep breath. Myocarditis and pericarditis can sometimes occur simultaneously, a condition termed myopericarditis, which presents with chest pain, shortness of breath, and palpitations.
Blood Clot Formation
COVID-19 infection can create a state of hypercoagulability, meaning the blood has an increased tendency to clot, which is a major source of chest pain. The systemic inflammation triggered by the virus can damage the endothelium, the inner lining of blood vessels, promoting clot formation. The virus uses the ACE2 receptor to enter cells, and this receptor is abundant on endothelial cells, suggesting a direct mechanism of vascular injury.
A clot that forms elsewhere, such as in the deep veins of the legs, can travel to the lungs and block an artery, causing a life-threatening pulmonary embolism (PE). A PE causes acute chest pain, often described as pleuritic, along with sudden shortness of breath and a rapid heart rate. Studies indicate that COVID-19 significantly increases the risk of venous thromboembolic events like PE, even in patients without other common risk factors.
Musculoskeletal Strain and Secondary Pain
Chest pain during a COVID-19 infection can also be purely mechanical or musculoskeletal in origin. The most common cause in this category is costochondritis, which is the inflammation of the cartilage connecting the ribs to the breastbone (sternum). This condition is often triggered by the severe, persistent coughing spells that frequently accompany a respiratory infection.
The pain associated with costochondritis is typically sharp, localized, and easily reproduced by pressing on the affected areas of the chest wall. This pain may also feel like a pressure or stabbing sensation that worsens with movement or deep inhalation. Beyond the cartilage, the intense effort of coughing can lead to generalized muscle soreness and strain in the chest and upper back, contributing to overall discomfort.