Sammy Zakaria, MD, MPH from Johns Hopkins University speaks about Acute Cardiac Effects of Severe Pre-Eclampsia.

Link to Article:
https://www.jacc.org/doi/10.1016/j.jacc.2018.04.048

Summary

Background: Pre-eclampsia with severe features (PEC) is a pregnancy-related condition marked by severe hypertension and end-organ dysfunction, as well as short-term adverse cardiovascular events such as heart failure, pulmonary edema, and stroke.

Objectives include:

The authors wanted to see how right ventricular (RV) systolic pressure (RVSP) and echocardiographic-derived diastolic, systolic, and speckle monitoring parameters changed over time in women with PEC.

Methodologies:

The authors enrolled 63 women with PEC and 36 pregnant control patients in this prospective retrospective study.

The following are the outcomes:

As compared to the control cohort, the PEC cohort had a higher RVSP (31.0 7.9 mm Hg vs. 22.5 6.1 mm Hg; p 0.001) and a lower global RV longitudinal systolic strain (RVLSS) (19.6 3.2 percent vs. 23.8 2.9 percent [p 0.0001]). There were significant differences (p 0.001) in mitral septal e′ velocity (9.6 2.4 cm/s vs. 11.6 1.9 cm/s), septal E/e′ ratio (10.8 2.8 vs. 7.4 1.6), left atrial area size (20.1 3.8 cm2 vs. 17.3 2.9 cm2), and posterior and septal wall thickness for left-sided cardiac parameters (median [interquartile range]: 1.0 cm [0.9 to 1.1 cm] vs. 0.8 cm [0.7 to 0.9 cm], and 1.0 cm [0.8 to 1.2 cm] vs. 0.8 cm [0.7 to 0.9 cm]). PEC was seen in eight women (12.7%) with grade II diastolic dysfunction and six women (9.5%) with peripartum pulmonary edema.

Final Thoughts:

When compared to healthy pregnant women, women with PEC have higher RVSP, higher rates of irregular diastolic activity, decreased global RVLSS, increased left-sided chamber remodeling, and higher rates of peripartum pulmonary edema.

Rozh H. Al-Mashhadi, MD from the Aarhus University Hospital discusses Local Pressure Drives Low-Density Lipoprotein Accumulation and Coronary Atherosclerosis in Hypertensive Minipigs.


Link to Research -
https://www.jacc.org/doi/10.1016/j.jacc.2020.11.059?utm_medium=social&utm_source=twitter_post&utm_campaign=twitter_post

Instract

Context
There is a limited understanding of the mechanisms by which hypertension accelerates coronary artery disease. There are sometimes confusing humoral changes in patients with hypertension, and to date, no experimental models have allowed the isolated effect of pressure on atherosclerosis to be studied in a setting that recapitulates the dimensions and biomechanics of human coronary arteries.

Targets
This thesis aimed to examine and explore the fundamental mechanisms of the impact of pressure on coronary atherosclerosis.

Methodology
Using inflatable suprarenal aortic cuffs, in the cephalad body portion of wild-type and hypercholesterolemic proprotein convertase subtilisin kexin type 9 (PCSK9)D374Y Yucatan minipigs, we increased mean arterial pressure by >30 mm Hg for >1 year. Pressures at the caudal remained natural.

Outcomes
Cephalad hypertension accelerated coronary atherosclerosis to nearly 5-fold under hypercholesterolemic conditions in transgenic PCSK9D374Y mini pigs, with the consistent development of fibroatheromas that were sufficiently large to induce computed tomography angiography stenosis. This was caused by local pressure forces since there were no changes in lesion formation in vascular beds shielded from hypertension but subjected to the same humoral influences. The same experiment was performed to investigate the underlying mechanisms under normocholesterolemic conditions in wild-type mini-pigs. Hypertension with increased abundance of mechanical strength proteins and decreased levels of infiltrating plasma macromolecules induced clear changes in the arterial proteome. Increased smooth muscle cells and increased intimate accumulation of low-density lipoproteins in the coronary arteries were parallel to this.

Findings
Coronary atherosclerosis is facilitated by elevated pressure per se. Our data show that redesign of the artery to balance higher tensile forces in hypertension changes the movement of macromolecules and contributes to the increased intimate accumulation of lipoproteins of low density.