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Left atrial (LA) dysfunction seems to play a central role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), is associated with disease severity and poor outcomes and potentially impacts management. Identifying LA myopathy can help guide tailored therapy for HFpEF. Echocardiography allows the accurate measurement of atrial size and function, where LA strain appears to be a sensitive measure of intrinsic LA myopathy. Several therapies and devices that decompress of left atrium are being tested for HFpEF. Further investigation is required to understand the specific atrial effects of statins, mineralocorticoid receptor antagonists, and other therapies.

Pulmonary hypertension (PH) is a progressive disease which is characterized with the increase of pulmonary artery pressure and pulmonary vascular resistance. Such condition leads to right ventricular heart failure and premature death of patients. Pulmonary arterial hypertension (PAH) has the status of an orphan disease. However in Russia only idiopathic PH is included in the list of 24 life-threatening and chronic progressive rare diseases, while other forms of PH are not in it. Inclusion in this list guarantees drug provision for patients at the expense of the regional budget, while patients with other forms of PH can rely on free medication only if they have a disability. The lack of criteria for revising this list as well as the imperfection of legal regulation in the field of drug support for orphan diseases leads to high disability, a significant decrease in the duration and quality of life of patients with PH. As part of a multicriteria approach, a clinical and economic analysis of the disease burden can be one of the tools for policy development and decision-making on the distribution of funding in the healthcare. The article provides a review of the economic burden of various forms of PH in the world.

The course of hypertension is often complicated by left ventricular hypertrophy (or hypertensive heart disease, HHD). The main “corridor” of natural HHD is development of heart failure with preserved ejection fraction (HFpEF). With HFpEF, the bioavailability of natriuretic peptides (NP) is significantly reduced, as a result of which the activity of cGMP-PKG signaling pathway, which plays a key role in maintaining normal diastolic function, weakens. It is possible to increase the activity of this pathway using the neprilysin inhibitor sacubitril. In case of HFpEF, the greatest efficacy from valsartan+sacubitril therapy should be expected in patients with severe concentric LVH, who have the most pronounced natriuretic peptide deficiency. Valsartan+sacubitril therapy has a clear hypotensive effect, causes a reversal of left ventricular hypertrophy and fibrosis. Since no effective treatment has yet been found for HFpEF, the main way for HHD treatment should be to prevent the diastolic dysfunction progression, which justifies valsartan+sacubitril therapy starting from the early/ asymptomatic stages.

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