Introdution: The purpose of this study was to investigate the mechanisms enrolled in the relationship between increased BP variability, heart damage and mortality in different pathophysiological conditions as hypertension, heart failure and myocardial infarction.
Method: Wistar rats were divided into control and S (n=10, 8weeks). Sinoaortic denervation (S) was performed using the method previously described. BP and HR were analysed using a data acquisition system. BP variability was analyzed by spectral analysis. Left ventricle systolic ejection and diastolic isovolumetric relaxation time were evaluated by echocardiography. Cardiac fibrosis and cardiomyocytes diameter were quantified by histological analysis. CO, cardiac blood flow and cardiac index were evaluated using colored microspheres.
Result: No difference was observed in BP and HR (C:104±2 vs 106±2 mmHg; C:313±7 vs 329±3 bpm), while BP variability was increased after S (C:29±2 vs 46*±5 mmHg). Left ventricle systolic ejection was decreased (C:72±0.9 vs 64*±1.5%) and diastolic isovolumetric relaxation time (C:21±1 vs 35*±1 ms) was increased in S group. Moreover, it was observed a reduction in CO (C:111±5 vs 81*±5 mL/min), an increase in cardiac resistance (C:35±1.8 vs 66*±2.6 mL/min/mmHg) and a decreased in cardiac index (C:320±9.7 vs 270*±8.1 l/min/m2) in S group. Those alterations resulted in decreased myocardial blood flow (C:3.47±0.21 vs 1.6*±0.3 mL/min/g). An increased cardiomyocytes diameter (C:14.9±0.3 vs 18.9*±0.3μm),fibrosis (C:0.85±0.08 vs 3.28*±0.2%) and cardiac hypertrophy index (C:3.07±0.06 vs 3.97*±0.1) were observed in S group.The association of all those changes lead to a 72% higher mortality in animals with increased blood pressure variability.(*p<0.03)
Conclusion: An increased BP variability resulted in a reduced cardiac blood flow, CO and cardiac index and an increased in myocardial resistance this adaptations occours as a attempt to homeostasis maintenance. Howerer, the morphofunctional alterations showed a diastolic dysfunction, increased cardiac hypertrophy index and fibrosis as a resulted. These adjustements could be a determinant factor in cardiac damage and in mortality in different pathological conditions, independently of BP levels.