Evaluation Of Heart Rate Fragmentation In Spontaneously Hypertensive Rats

Rapid heart rate (HR) variations at respiratory frequency range are well accepted as a marker of cardiac vagal modulation. Nevertheless, a new pattern of ultra-rapid HR variation has been recently studied and named as heart rate fragmentation (HRF). HRF is a type of sinoatrial instability characterized by the presence of numerous inflections points (from one bit to another) in RR interval time series. HRF has been shown to be increased in aging and coronary diseases and seems to be linked to the risk life-threatening cardiovascular events and death. This study aimed to evaluate the HRF in a rat model of spontaneous hypertension. Unanesthetized freely moving spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats at 2 distinct ages, 4 to 6 weeks (young) or 12 to 15 weeks (adult), had their electrocardiogram recorded for 40 minutes. Series of RR intervals were generated and transformed into a sequence of symbols “-1”, “0” or “1” when the difference between successive RR values (transitions) was positive, zero, or negative, respectively. Transitions between symbols “-1” and “1” were labeled as “hard” (H) inflection points while those between “-1” (or “1”) and “0” were labeled as “soft” (S) inflection points. Next, sequences of 4 consecutive symbols (words - W) were distributed according to the number and type of transition they enclose. The total percentage of inflection points (PIP), the percentage of words with zero (W0), one (W1), two (W2) or three (W3) inflection points, as well as percentage of words enclosing only hard (WH), soft (WS) or mixed (WM), i.e., containing both types of inflection points, were quantified. PIP and W3 were lower in the young and adult SHR when compared to the counterparts WKY. In contrast, young and adult SHR showed a higher percentage of W0, W1 and W2 compared to WKY.Regarding the type of transition, the percentage of WH was lower, while the WS was higher, in young and adult SHR when compared to WKY counterparts. The percentage of WM was higher only in young SHR. In conclusion, although evidences indicate that cardiovascular diseases lead to an increase in HRF, we have shown lower HRF in hypertensive rats, with or without the presence of the hypertensive phenotype. However, the mechanisms giving rise to HRF are still unknown. Future studies must be conducted to evaluate whether the HRF pattern observed in young and adult SHR is maintained in elderly animals and to elucidate the mechanisms behind HRF in SHR and normotensive rats.