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State of the Art lecture. Risk mechanisms in hypertensive heart disease
1Alton Ochsner Medical Foundation, New Orleans, LA 70121, USA.
Insights
Hypertensive heart disease and left ventricular hypertrophy involve coronary hemodynamic changes, endothelial dysfunction, and fibrosis. These alterations increase the risk of serious cardiac events like heart attack and failure.
Area of Science:
- Cardiology
- Pathophysiology
Background:
- Hypertensive heart disease and left ventricular hypertrophy (LVH) present independent cardiovascular risks.
- Key pathophysiological alterations include altered coronary hemodynamics and endothelial dysfunction.
Discussion:
- Classically described coronary hemodynamic changes include reduced coronary blood flow and flow reserve, alongside increased coronary vascular resistance.
- Emerging concepts highlight the role of endothelial dysfunction.
- Increased collagen deposition (fibrosis) in ventricular walls and perivascularly contributes significantly to cardiac dysfunction.
Key Insights:
- Aging and high salt intake can exacerbate these cardiac changes.
- Functional and structural alterations lead to worsening endothelial dysfunction, impaired coronary hemodynamics, and compromised systolic and diastolic ventricular function.
Outlook:
- Clinical consequences encompass angina, myocardial infarction, cardiac failure, lethal arrhythmias, and sudden cardiac death.
- LVH is not solely myocytic hypertrophy; it involves comorbid changes like fibrosis, impaired hemodynamics, and endothelial dysfunction that elevate cardiac risk.
Abstract:
In this report, some of the underlying pathophysiological alterations associated with the independent risk from hypertensive heart disease and left ventricular hypertrophy are discussed. Emphasized are the classically described coronary hemodynamic alterations of decreased coronary blood flow and flow reserve with increased coronary vascular resistance and minimal coronary resistance; more recent concepts of endothelial dysfunction are emphasized. Additionally, increased collagen deposition within the ventricular walls and perivascularly participates importantly. These changes are exacerbated by the aging process and perhaps by increased dietary salt intake. Consequences of these functional and structural changes include further endothelial dysfunction, impairment of coronary hemodynamics, and ventricular contractile function (diastolic as well as systolic). The clinical consequences of these alterations are angina pectoris (with or without atherosclerosis), myocardial infarction, cardiac failure, lethal dysrhythmias, and sudden cardiac death. Thus, not all that is clinically recognized as "left ventricular hypertrophy" is true myocytic hypertrophy with structural remodeling; other important comorbid changes occur that directly affect risk, including ventricular fibrosis, impaired coronary hemodynamics, and endothelial dysfunction.