Related Experiment Videos
Prevention of atherosclerosis and end-organ damage: a basis for antihypertensive interventional strategies
C J Schwartz1, A J Valente, E F Hildebrandt
1Department of Pathology, Graduate School of Biomedical Sciences, University of Texas Health Science Center, San Antonio 78284-7750.
Insights
Essential hypertension and coronary heart disease share complex origins, necessitating early intervention. Blood pressure variability significantly impacts cardiovascular end-organ damage in hypertensive patients.
Area of Science:
- Cardiovascular Medicine
- Hypertension Research
- Atherosclerosis Pathogenesis
Background:
- Essential hypertension is a major risk factor for cardiovascular end-organ damage, particularly coronary heart disease.
- Atherosclerosis and hypertension originate in childhood, with advanced plaque development accelerating in early adulthood.
- Complex interrelationships exist between hypertension and key coronary heart disease risk factors like hyperinsulinemia, insulin resistance, and dyslipidemia.
Purpose of the Study:
- To review the intricate links between essential hypertension and cardiovascular end-organ damage.
- To focus on the pathogenesis and prevention of coronary heart disease as a primary complication of untreated hypertension.
- To highlight the role of blood pressure variability in hypertensive end-organ damage.
Main Methods:
- Review of existing literature on hypertension, atherosclerosis, and cardiovascular disease.
- Analysis of cellular and molecular mechanisms in atherogenesis, including monocyte-macrophages, oxidant stress, and inflammation.
- Evaluation of the impact of experimental hypertension on atherogenesis and arterial wall permeability.
- Assessment of antihypertensive therapy's effect on blood pressure variability using the trough: peak ratio.
Main Results:
- Hypertension significantly accentuates atherogenesis, affecting cervical and cerebral arteries.
- Acute hypertension can increase arterial wall permeability to plasma proteins.
- Twenty-four-hour blood pressure variability correlates with target-organ damage in hypertensive individuals.
- Antihypertensive therapy should address both blood pressure levels and short-term fluctuations.
Conclusions:
- Further intensive research is needed to fully elucidate the relationship between hypertension and atherogenesis.
- Early diagnosis and intervention are crucial due to the early onset of hypertension and atherosclerosis.
- Understanding the cellular and molecular pathways is key to preventing hypertension-related cardiovascular complications.
Aim:
To review the nature of the complex relationships between essential hypertension and cardiovascular end-organ damage, with a particular focus on the pathogenesis and prevention of coronary heart disease, the major complication of untreated hypertension. RISK FACTORS FOR CORONARY HEART DISEASE: Both atherosclerosis and hypertension have their origins in childhood; in the second and third decades of life development of the more advanced fibrous plaques accelerates, emphasizing the need for early diagnosis and intervention. Perplexing and complex relationships have been found among the principal risk factors for coronary heart disease, hyperinsulinemia, insulin resistance, dyslipidemia and hypertension. In the pathogenesis of atherosclerosis at the cellular and molecular level, the important features are the effects of monocyte-macrophages, oxidant stress, lipoprotein modification, inflammatory mediators and the focal hemodynamic environment. Even brief periods of experimental hypertension can accentuate atherogenesis, the effects of which are greatest but not limited to the cervical and cerebral arteries. Further, acute hypertension lasting for even a few minutes causes a 'leakage' of plasma proteins and particulate probes into the artery wall, which has far-reaching implications for antihypertensive therapy. Recent work has shown that 24-h blood pressure variability is correlated with target-organ damage in hypertensive patients.
Therapy:
Antihypertensive therapy should not only lower blood pressure but also prevent significant short-term blood pressure fluctuations. The trough: peak ratio has been used to assess the effect of antihypertensive treatment on blood pressure variability.
Conclusion:
More intensive research is required to clarify the nature of the interface between hypertension and atherogenesis.