Sex chromosomes and hormones influence blood pressure regulation, cardiovascular risk factors and co-morbidities in a gender specific manner. As a result, males and females with essential arterial hypertension may require different treatment and management. However, not enough sex-specific clinical trial data exist to illustrate how these sex-specific blood pressure differences should be managed. As a result, several European medical associations collaborated on a scientific statement addressing these disparities. The resulting collaborative document entitled “Sex differences in arterial hypertension,” was recently published in the European Heart Journal.
The scientific statement provides a comprehensive review of the latest data on sex-specific contrasts in essential arterial hypertension, CV disease (CVD), and hypertension management. The document also undertakes to identify knowledge gaps limiting the development of hypertension management strategies based specifically on sex. Some of the document’s highlights follow.
Understanding differences in blood pressure in males and females
As the scientific statement asserts, the development of blood pressure and hypertension differs between the sexes. Males and females begin with similar levels of systolic blood pressure (SBP) and diastolic BP (DBP); however, around age of 13 years, BPs start to diverge. Through adulthood, SBP measurements are lower in females, while males experience higher DBPs. These aspects remain unchanged into middle age; however, once past midlife, the transition from optimal BP to hypertension increases rapidly in females while it stabilizes or decreases in males. Therefore, understanding how SBP and DBP evolve differently for females and males over their lifetimes is crucial to preventing—and managing—hypertension.
Recognizing differences in blood pressure regulators, CV risk, and co-morbidities
The scientific statement authors acknowledge that variations in blood pressure regulators, CV risk factors and co-morbidities exist between the sexes. For instance, sex chromosomes, sex hormones and other autonomic nervous system hormones strongly influence the autonomic and endocrine blood pressure regulators. These in turn alter how males and females synthesize and react to drugs differently, including how adverse events are manifested. Understanding why males achieve better BP control than females with the same antihypertensive medication is crucial to managing hypertension effectively.
Sex-specific differences in CV risk factors and co-morbidities are well documented, yet CVD risk assessment tools don’t distinguish between them. As such, the collaborative document encourages integrating these sex-specific variances into risk assessments, thereby refining CVD prevention. Besides, identifying those underlying mechanisms of CVD progression in both sexes may alter target thresholds used to determine treatment, etc.
Regarding blood pressure associated with CVD, CV risks tend to increase at a lower blood pressure level in females than in males. Additionally, females with hypertension develop atrial fibrillation (AF) and HF with preserved ejection fraction (HFpEF); males with hypertension, on the other hand, experience more often HF with reduced EF (HFrEF) and acute myocardial infarction (AMI).
Awaiting clinical and guideline adoptions of sex-difference evidence
These sex-specific disparities between blood pressure and hypertension expose the need for guidelines recommending sex-based strategies rather than “one-size-fits-all” approaches. However, the knowledge gaps in understanding these differences between males and females in CVD progression linger; therefore, it is crucial to identify the underlying mechanisms for sex-specific CV organ damage development. Consequently, the scientific statement authors concluded, further clinical studies must determine if using sex-specific threshold values can expand CVD prevention.
For more cardiology research news join our newsletter or follow us on Twitter, Facebook, LinkedIn or Instagram.
Author: Saskia van Tetering
Original Article: Gerdts E et al. Eur Heart J. 2022;00:1-12.