Beta-blockers in Hypertensive Left Ventricular Hypertrophy and Atrial Fibrillation Prevention.

BACKGROUND: Hypertensive left ventricular hypertrophy (HTN LVH) is a key risk factor for atrial fibrillation (AF). OBJECTIVE: To evaluate the possible role of beta-blockers (BBs) in addition to a renin-angiotensinaldosterone system (RAAS) blocker in AF prevention in patients with HTN LVH. METHODS: We performed a PubMed, Elsevier, SAGE, Oxford, and Google Scholar search with the search items 'beta blocker hypertension left ventricular hypertrophy patient' from 2013-2023. In the end, a 'snowball search', based on the references of relevant papers as well as from papers that cited them was performed. RESULTS: HTN LVH is a risk factor for AF. In turn, AF substantially complicates HTN LVH and contributes to the genesis of heart failure (HF) with preserved ejection fraction (HFpEF). The prognosis of HFpEF is comparable with that of HF with reduced EF (HFrEF), and, regardless of the type, HF is associated with five-year mortality of 50-75%. The antiarrhythmic properties of BBs are wellrecognized, and BBs as a class of drugs are - in general - recommended to decrease the incidence of AF in HTN. CONCLUSION: BBs are recommended (as a class) for AF prevention in several contemporary guidelines for HTN. LVH regression in HTN - used as a single criterion for the choice of antihypertensive medication - does not capture this protective effect. Consequently, it is worth studying how meaningful this antiarrhythmic action (to prevent AF) of BBs is in patients with HTN LVH in addition to a RAAS blocker.

Beta Blockers can Mask not only Hypoglycemia but also Hypotension.

BACKGROUND: Beta-adrenergic (ß-AR) receptor blockers (BBs) are an essential class of drugs as they have numerous indications. On the other hand, they have numerous unwanted effects that decrease the compliance, adherence, and persistence of this very useful group of drugs. OBJECTIVE: The paper aims to analyze the possibility that an unnoticed side effect may contribute to a less favorable pharmacologic profile of BBs, e.g., a diminished reaction to a sudden fall in BP. METHODS: We searched two medical databases for abstracts and citations (Medline and SCOPUS). Moreover, we searched the internet for drug prescription leaflets (of the individual BBs). RESULTS: Whichever cause of stress is considered, the somatic manifestations of stress will be (partially) masked if a patient takes BB. Stress-induced hypercatecholaminemia acts on ß-AR of cardiomyocytes; it increases heart rate and contractility, effects suppressed by BBs. The answers of the organism to hypoglycemia and hypotension share the main mechanisms such as sympathetic nervous system activation and hypercatecholaminemia. Thus, there is a striking analogy: BBs can cover up symptoms of both hypoglycemia (which is widely known) and of hypotension (which is not recognized). It is widely known that BBs can cause hypotension. However, they can also complicate recovery by spoiling the defense mechanisms in hypotension as they interfere with the crucial compensatory reflex to increase blood pressure in hypotension. CONCLUSION: Beta blockers can cause hypotension, mask it, and make recovery more difficult. This is clinically important and deserves to be more investigated and probably to be stated as a warning.

Relation of atrial fibrillation and right-sided cardiac thrombus to outcomes in patients with acute pulmonary embolism.

Atrial fibrillation (AF) can induce a hypercoagulable state in both the left and right atria. Thrombus in the right side of the heart (RHT) may lead to acute pulmonary embolism (APE). The aim of the study was to determine the prevalence of RHT and AF and to assess their impact on outcomes in patients with APE. The retrospective cohort included 1,006 patients (598 female), with a mean age of 66 ± 15 years. The primary end point was all-cause mortality. The secondary end point was incidence of complications (death, cardiogenic shock, cardiac arrest, vasopressor/inotrope treatment, or ventilatory support). Atrial fibrillation was detected in 231 patients (24%). RHT was observed in 50 patients (5%). The combination of AF and RHT was observed in 16 patients (2%). The overall mortality rate was significantly higher in patients with RHT compared with those without (32% vs 14%, respectively, odds ratio [OR] 3.0, 95% confidence interval [CI] 1.6 to 5.6, p = 0.001). The rate of complications was significantly higher in patients with RHT in comparison to those without (40% vs 22%, respectively, OR 2.4, 95% CI 1.3 to 4.4, p = 0.004). The mortality rate in patients with both AF and RHT was significantly higher in comparison to those with AF but without RHT (50% vs 20%, respectively, OR 3.86, 95% CI 1.3 to 11.2, p = 0.01). In multivariate analysis, RHT (p = 0.03) was an independent predictor of death. In conclusion, AF is a frequent co-morbidity in patients with APE, and the presence of RHT is not uncommon. Among patients with APE, the presence of RHT increases the mortality approximately threefold regardless of the presence of known AF.