Comorbidity in chronic obstructive pulmonary disease and cardiovascular disease

Abstract

Comorbidity is one of the most significant problems of modern healthcare. Numerous studies have analyzed the possible pathogenetic mechanisms and relationships between a wide variety of diseases. Cardiovascular (CVD) and pulmonary diseases, in particular chronic obstructive pulmonary disease (COPD), have a number of the same risk factors and pathogenetic links, which aggravate each other's course. Moreover, CVD and COPD are among the most common diseases in the world. This review provides up-to-date information on the prevalence, risk factors and pathophysiological mechanisms underlying this unfavorable combination of diseases. Some problems of diagnosis and treatment of patients with COPD and CVD are also discussed.

The Main Causes and Mechanisms of Increase in Cardiac Troponin Concentrations Other Than Acute Myocardial Infarction (Part 1): Physical Exertion, Inflammatory Heart Disease, Pulmonary Embolism, Renal Failure, Sepsis

“…It is assumed that in nonmassive PE, reversible damage of RV cardiomyocytes and release of cytosolic troponins pool through the cell membrane due to increased afterload occur. 86,87 In submassive and massive PE, RV overload is much more pronounced and cardiomyocyte necrosis develops. Probably the cause of cardiac myocyte necrosis in PE are sharp overload and expansion of RV, which might lead to compression of small branches of coronary arteries, passing in myocardial tissue thickness, causing disruption of hemoperfusion and delivery of oxygen and metabolic substrates to myocardial cells.…”

Elevation Mechanisms and Diagnostic Consideration of Cardiac Troponins under Conditions Not Associated with Myocardial Infarction. Part 1

“…The mechanisms of increasing cardiac troponins in non-massive PE are most likely associated with the release of the cytosolic pool through the membrane of the right ventricular cardiomyocytes, due to increased afterload, which is similar to how it occurs during intense physical exertion [67][68][69]. In the case of submassive and massive PE, necrosis of cardiomyocytes happens.…”

Cardiac Troponins Metabolism: From Biochemical Mechanisms to Clinical Practice (Literature Review)

“…It has been shown that the heart rate, blood pressure, vascular resistance, prothrombotic tendency, platelet aggregation ability, activity of the renin-angiotensin-aldosterone system, activity of the sympathoadrenal system, and levels of catecholamines and cortisol increase in the morning hours, which have evolved and are necessary for normal functioning in the period of wakefulness. However, this has important implications for the pathophysiology of cardiovascular diseases: the frequency of cardiovascular accidents is significantly higher in the morning hours [113][114][115][116][117][118]. The maximum number of cases of AMI occurs in the morning-afternoon time interval (8:00-12:00).…”