Psoriasis, a widely prevalent chronic disease of the skin and joints, has long been associated with far-reaching systemic ramifications and decreased quality of life. However, psoriasis is largely underdiagnosed and insufficiently treated. Classical risk factors predisposing to cardiovascular diseases, such as hypertension, diabetes, metabolic syndrome, and dyslipidemia, have been noted in patients with mild and severe psoriasis. Furthermore, the magnitude of the cardiovascular comorbidity and the need to screen for risk factors has often been ignored while considering the management options for psoriasis. This article has reviewed the cardiovascular implications of psoriasis from the shared pathogenesis behind these two diseases to the increased incidence of cardiovascular events, such as myocardial infarction, stroke, and other causes of vascular mortality. Additionally, the therapeutic targets of common inflammatory pathways, such as those involving tumor necrosis factor α (TNF-α), interleukin-12/interleukin-23 (IL-12/IL-23), and helper T cells 17 (Th17), have been discussed with an emphasis on their efficacy in controlling psoriasis and its cardiovascular consequences.

Chronic pain is known as ongoing pain that lasts longer than three months with increasing healing time. It is approximated that 20% of adults of different sexes, races, and socioeconomic backgrounds fall victim to chronic pain. It is a result of several factors and can have lifelong effects. Pain is a complex matter to measure; therefore, the physician needs to understand the patient’s health state to create a management plan tending to each issue adequately. There are many complications of such pain, and it can interfere terribly with an individual’s quality of life. This article has reviewed the complex pathogenesis of chronic pain and the spectrum of non-pharmacologic modalities and pharmacological treatment options. It has also explored the efficacy of certain drugs and underlined the importance of nonpharmacological options such as physical exercise, cognitive therapy, and physical modalities to treat chronic pain and all the conditions that accompany this disorder.

Migraines are one of the emerging causes of disabilities experienced worldwide, and strokes are the second leading cause of death globally. Migraines with aura have been reported to be associated with a higher risk of ischemic strokes, whereas hemorrhagic strokes are more closely associated with migraines without aura, possible mechanisms that link migraines to strokes. These can be categorized into vascular mechanisms such as vasospasm, endothelial and platelet dysfunction, and alteration in the vessel wall seen in migraineurs, further perpetrated by vascular risk factors such as hypertension and hyperlipidemias. Cerebral hypoperfusion that occurs in migraines can cause an electrical aberrance, leading to a phenomenon known as "spreading depression" which can contribute to strokes. In this review, we discuss bloodstream elevation in procoagulants such as antiphospholipid antibodies, homocysteine, von Willebrand factor, and prothrombin. Maintaining pregnant women who actively experience migraines with aura under close observation may be of some value in achieving better outcomes. Women who experience migraines after starting hormonal contraception are at a higher risk of experiencing strokes and stand to benefit from being switched to non-hormonal methods. In this article, we discuss the mechanisms linking migraines and strokes, briefly discuss the pathogenesis, and explore the risk factors contributing to the association therein. In addition, we examine the relationship between migraines and ischemic strokes, as well as hemorrhagic strokes, and review management considerations.

Thyrotoxicosis is a clinical syndrome with persistently elevated concentrations of free triiodothyronine, free thyroxine, or both, which correlates with an increased thyroid metabolic function. This article has discussed the direct effect of increased thyroid hormone on the heart, as the thyroid hormone physiologically exhibits a close harmony with hormones of the cardiovascular system. This action can lead to disturbances in hemodynamic stability, exacerbating the possibility of developing complications such as heart failure and life-threatening arrhythmias. This article has also explored the multifaceted pathogenesis of thyrotoxicosis and various pharmacological treatment options, including beta-blockers and anti-thyroid drugs. This article has reviewed numerous studies that have concluded that the main goal of therapy should always aim to normalize thyroid hormone levels based on the etiology of the thyrotoxicosis, although cardiovascular conditions are associated with a higher rate of mortality.

Heart failure is a clinically complex syndrome that results due to the failure of the ventricles to function as pump and oxygenate end organs. The repercussions of inadequate perfusion are seen in the form of sympathetic overactivation and third spacing, leading to clinical signs of increased blood pressure, dyspnea, fatigue, palpitations, etc. This article provided a brief overview of the clinical syndrome of heart failure; its epidemiology, risk factors, symptoms, and staging; and the mechanisms involved in disease progression. This article also described several landmark trials in heart failure that tested the efficacy of first-line drugs such as beta-blockers, angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and the latest drugs in the field of heart failure: angiotensin receptor neprilysin inhibitors. Most studies described in this article were guideline-setting trials that revolutionized the practice of medicine and cardiology.