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The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in
Clovis de Carvalho Frimm1, Valéria F A Pereira, Ana Clara T Rodrigues
1Emergências Clínicas (LIM 51), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil. frimm@emercli.fm.usp.br
Insights
Myocardial supply-demand imbalance worsens cardiac dysfunction in hypertension. Reduced coronary reserve/stress is linked to decreased fractional shortening, indicating impaired cardiac performance.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Cardiac Dysfunction
Background:
- The role of coronary reserve impairment in hypertensive cardiac dysfunction remains debated.
- Previous findings showed coronary vasodilation can coexist with systolic dysfunction.
- Inappropriate coronary reserve for heightened myocardial oxygen demand may negatively impact cardiac performance.
Purpose of the Study:
- To investigate if myocardial supply-demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN).
- To assess the relationship between coronary reserve, end-systolic stress, and cardiac function in hypertensive individuals.
Main Methods:
- Echocardiography was used to determine fractional shortening and end-systolic stress.
- Transesophageal Doppler echocardiography calculated coronary reserve.
- Coronary reserve/stress ratio served as a supply-demand measure in healthy subjects (NL) and hypertensive patients (HTN1-3) with varying fractional shortening.
Main Results:
- Hypertensive groups HTN2 and HTN3 exhibited significantly greater end-systolic stress compared to NL and HTN1.
- Coronary reserve was only impaired in HTN3, but coronary reserve/stress was reduced in both HTN2 and HTN3.
- Diastolic internal dimension, end-systolic stress, and coronary reserve/stress independently correlated with fractional shortening.
Conclusions:
- Supply-demand imbalance explains the severity of cardiac dysfunction in hypertension.
- This imbalance provides additional insight into cardiac enlargement and elevated wall stress in hypertensive heart disease.
Background:
The pathophysiologic role of coronary reserve impairment in hypertensive cardiac dysfunction is still debated. Previously, we demonstrated that satisfactory coronary vasodilatation may coexist with ventricular systolic dysfunction. It is conceivable that coronary reserve might otherwise be inappropriate for enhanced myocardial oxygen demand and may thus affect cardiac performance negatively.
Hypothesis:
Myocardial supply-demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN).
Methods:
Fractional shortening (%) and end-systolic stress (10(3) x dyn x cm(-2)) were determined using echocardiography, and coronary reserve was calculated using transesophageal Doppler echocardiography. Coronary reserve/stress (cm2 x dyn(-1)) was utilized as a measure of supply-demand. Groups NL (20 healthy subjects), HTN1 (15 patients, fractional shortening > or = 30), HTN2 (19 patients, 20 < or = fractional shortening < 30), and HTN3 (21 patients, fractional shortening < 20) were constituted.
Results:
Compared with NL and HTN1, groups HTN2 and HTN3 had significantly (p < 0.05) greater end-systolic stress (NL = 72 +/- 16, HTN1 = 72 +/- 23, HTN2 = 143 +/- 32, HTN3 = 186 +/- 70). Coronary reserve was impaired in HTN3 alone (NL = 3.5 +/- 0.6, HTN1 = 3.4 +/- 1.0, HTN2 = 3.1 +/- 1.0, HTN3 = 2.6 +/- 1.1), but coronary reserve/stress was reduced in both HTN2 and HTN3 (NL = 50 +/- 12, HTN1 = 53 +/- 21, HTN2 = 22 +/- 7, HTN3 = 15 +/- 7). Stepwise regression analysis identified diastolic internal dimension, end-systolic stress, and coronary reserve/stress as independently associated with fractional shortening.
Conclusion:
The imbalance between supply-demand explains the severity of hypertensive cardiac dysfunction and adds information to cardiac enlargement and elevated wall stress.
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