Pneumonia caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first time reported on December 31, 2019. 1 Since then, the COVID-19 pandemic, disease caused by this virus, had spread around the world. Until April 10, over 1.6 million confirmed cases in total and almost 100 000 deaths were identified worldwide. Everything started from Wuhan, Hubei Province, in China more than 4 months ago, and therefore practically, all relevant clinical data are coming from China. These findings are showing that arterial hypertension, diabetes, cardiovascular diseases, and chronic obstructive pulmonary disease are common comorbidities in patients with COVID-19 2-22 (Tables 1 and 2). Even though the number of studies with follow-up is rather limited, these data are suggesting that hypertension, diabetes, and cardiovascular disease are underlying conditions associated with adverse outcome-admission in intensive care unit, mechanic ventilation, and death [6][7][8][9]13,18 (Table 3). However, findings are inconsistent and data are more epidemiological than analytical. Majority of studies did not analyze effect of many confounding factors, such as age, sex, and obesity, which could significantly change interaction between comorbidities and outcome. It is clear that sudden outbreak of COVID-19 raised a great attention and forced rapid publication in order to explain epidemiology, therapeutic approach, and outcome. Many parameters were not available, and inclusion of some risk factors, such as obesity, that would probably interfere with final results was not possible so far. Therefore, one should be careful in interpretation of available data and indicating hypertension and diabetes as one of the most responsible risk factors, at least not in global population.The aim of this review was to summarize currently available data regarding the prevalence of diabetes in patients with COVID-19 and its role in outcome in these patients. Hence, a comprehensive systematic search was performed on PubMed, Scopus, Web

Arterial hypertension and stroke are strong independent risk factors for the development of cognitive impairment and dementia. Persistently elevated blood pressure (BP) is known to impair cognitive function, however onset of new cognitive decline is common following a large and multiple mini strokes. Among various forms of dementia the most prevalent include Alzheimer’s disease (AD) and vascular dementia (VaD) which often present with similar clinical symptoms and challenging diagnosis. While hypertension is the most important modifiable vascular risk factor with antihypertensive therapy reducing the risk of stroke and potentially slowing cognitive decline, optimal BP levels for maintaining an ideal age-related mental performance are yet to be established. Cognition has improved following the use of at least one representative agent of the major drug classes with further neuroprotection with renin angiotensin inhibitors and calcium channel blockers in the hypertensive elderly. However, a reduction in BP may worsen cerebral perfusion causing an increased risk of CV complications due to the J-curve phenomenon. Given the uncertainties and conflicting results from randomized trials regarding the hypertension management in the elderly, particularly octogenarians, antihypertensive approaches are primarily based on expert opinion. Herein, we summarize available data linking arterial hypertension to cognitive decline and antihypertensive approach with potential benefits in improving cognitive function in elderly hypertensive patients.

The coronavirus disease (COVID-19) has spread all around the world in a very short period of time. Recent data are showing significant prevalence of arterial hypertension and cardiovascular diseases (CVD) among patients with COVID-19, which raised many questions about higher susceptibility of patients with these comorbidities to the novel coronavirus, as well as the role of hypertension and CVD in progression and the prognosis of COVID-19 patients. There is a very limited amount of data, usually obtained from a small population, regarding the effect of the underlying disease on the outcome in patients with COVID-19. The evaluation of the treatment of these comorbidities at baseline and during COVID-19 is scarce and the results are conflicting. Hypertension and CVD, after the adjustment for other clinical and demographic parameters, primarily age, did not remain independent predictors of the lethal outcome in COVID-19 patients. Some investigations speculated about the association between the renin-angiotensin-aldosterone system (RAAS) and susceptibility to COVID-19, as well as the relationship between RAAS inhibitors and the adverse outcome in these patients. Withdrawing or switching RAAS inhibitors would have uncertain benefits, but it would definitely have many disadvantages such as uncontrolled hypertension, cardiac function deterioration and renal function impairment, which could potentially induce more complications in patients with COVID-19 than the infection of coronavirus itself. The aim of this review article was to summarize the prevalence of hypertension and CVD in patients with COVID-19, their influence on the outcome and the effect of treatment of hypertension and CVD in COVID-19 patients.

Reverse or inverted dipping (ie, the phenomenon characterized by higher nighttime compared with daytime blood pressure values) is an alteration of circadian blood pressure rhythm frequently documented in hypertension, type 2 diabetes mellitus, chronic kidney disease, and sleep apnea syndrome, and generally regarded as a harmful condition. Available literature on the clinical and prognostic implications of reverse dipping is scanty. The present article will review a number of relevant issues concerning reverse dipping, in particular: (1) its possible mechanisms; (2) prevalence and clinical correlates, (3) concomitant cardiac and extracardiac subclinical organ damage; (4) association with acute and chronic cardiovascular diseases; (5) prognostic value in predicting cardiovascular events and mortality; and (6) therapeutic interventions aimed at reverting this abnormal circadian blood pressure rhythm.

The coronavirus disease 2019 (COVID-19) may cause not only an acute respiratory distress syndrome (ARDS) but also multiple organ damage and failure requiring intensive care and leading to death. Male sex, advanced age, chronic lung disease, chronic kidney disease and cardiovascular disease, such as hypertension, diabetes and obesity have been identified as risk factors for the COVID-19 severity. Presumably, as these three cardiovascular risk factors are associated with a high prevalence of multiorgan damage. In the present focused clinical review, we will discuss the cardiovascular complications of COVID-19 including acute cardiovascular syndrome (acute cardiac injury/COVID cardiomyopathy, thromboembolic complications and arrhythmias) and post-COVID-19 sequelae. Preliminary data shows that the cause of acute cardiovascular syndrome may be multifactorial and involve direct viral invasion of the heart and vascular system, as well as through the immune and inflammation-mediated systemic cytokine storm. COVID-19 survivors may also show persistently elevated blood pressure and sinus tachycardia at rest. Furthermore, poor diabetic control, persistent renal damage and cerebral sequelae, such as persistent cognitive and neuropsychiatric alterations are also frequently reported. A particular attention should be paid towards cardiovascular protection in COVID-19 patients who develop acute cardiovascular syndromes during hospitalization, and/or permanent/semipermanent sequelae after recovery from COVID-19. These conditions may require careful clinical assessment, treatment and close follow-up to avoid short-term and long-term complications.