**1. Introduction**

The cardiovascular control system (CVCS) – the heart, the vessels and the brain – executes optimum performance of the blood circulation if it works under a healthy condition. If CVCS is defective, the heart contractions lose any useful rhythm, for example, like as patient who is suffering from sinus node dysfunction. It is ideal to identify the causes of defectiveness by existing diagnostic methods.

The discovery of the circulation of the blood (William Harvey in 1628) was a long time ago. But until recently, we do not know about what is the proper behaviour of CVCS. In 1982, Kobayashi and Musha reported and determined that a healthy heart exhibits a 1/f spectrumlike fluctuation [1]. 1/f fluctuations are widely found in nature (beginning, Johnson and Nyquist noise, 1920s). Until now, 1/f rhythm of healthy hearts has become a widely held

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons

notion [2, 3]. We consider that 1/f spectrum is a state where, mathematically, scaling exponent (SI) is 1.0. We have, therefore, made a time series analysis programme in order to check the heartbeat wellness: computing whether or not a time series exhibits SI = 1.0. Our technique is a random-walk analysis, which calculates 'the number of steps proceeded within a box, i.e., increased or decreased' [4, 5]. The name of the method is mDFA (abbreviated name, modified detrended fluctuation analysis). We have explained it elsewhere, about the box, steps and entrance and the exit of a box, and so on [4, 5]. As a result, our method showed that SI can quantify the condition of CVCS [4, 5]. This quantification is like the thermometer. It has a baseline value. If the body condition is normal, it is 37°.

In particular, as far as we know, the association of high SI with unpredictable cessation of heart pumping has been discovered. It has not been shown empirically before us. We first observed it in the crustacean heart; thereafter, we confirmed the same phenomena (high SI) on humans with ischaemic disease and a person who underwent a surgery that made an incision of the heart [4, 5].

By the way, our heart rhythm is apparently not regular. Cardiac rhythmicity is continuously changing, because CVCS is responding to stimulus from the internal and outer world. Therefore, marked irregularity and/or over-regularity might be a deficient state. At least mDFA seems to detect defect/problem that derives from an injury of the myocardial cells caused by either ischaemic reasons or artificial/synthetic reasons. It seems that mDFA is a better way to compute this correlation between an SI value and a poor condition of CVCS.

Lower animals such as crustaceans have a heart. Crustacean CVCS has been well studied over 100 years. For example, the English comparative biologist-anatomist Tomas Henry Huxley published about crayfish zoology in ca. 1900s [6]. And Swedish American physiologist Anton Julius Carlson has already documented detailed morphology and physiology of the heart of horseshoe crabs (*Limulus polyphemus*), in 1904 [7]. It is worth noting that Carlson already considered invertebrate hearts as a model of our heart.

Until now, the anatomy of cardiac nerve of crustaceans is well documented. The crustacean animal has autonomic nervous system that controls the heart (see Cooper et al., e.g. [8], and legendary articles [9, 10]). Typically, crustacean heart is innervated by two acceleratory nerves and one inhibitory nerve (**Figure 1**, see [11]). **Figure 2** shows a diagrammatical view of cardiac nerves in both vertebrates and crustaceans. Crustacean diagram is based on our publication [11]. In summary, the cardiac inhibitory nerve innervates pacemaker cells (P in **Figure 2**) in both crustaceans and humans. In turn, the cardiac acceleratory nerve innervates not only P cells but also myocardial cells (ventricle cells). As shown in **Figure 2**, it is important to acknowledge that nerve fibres of accelerator (CA) proceed deep inside the heart. This fact presents evidence that CA nerve regulates not only the rhythm of the heart but also the strength of heart contraction. **Figure 2** highlights an important issue in terms of evolution: the heart and its controller system resemble in both invertebrate and vertebrate. Further discussions about the resemblance are shown in Ref. [4]. Thus, we strongly expect that a basic finding obtained from invertebrate animals is applicable to humans, according to an evolutional view [4].

Anxiety, Worry and Fear: Quantifying the Mind Using EKG Time Series Analysis http://dx.doi.org/10.5772/intechopen.71041 9

**Figure 1.** Crustacean CVCS. Autonomic-like regulation of the heart. Cardio-regulatory nerves are the following: ci, cardio-inhibitory nerve, ca, cardio-acceleratory nerve, dcn, bilateral dorsal cardiac nerves. A dcn carries only three nerve axons, one ci and two ca nerves. Arrows, the direction of blood flow. Blood is pumped out from the heart (h), all meeting at the gill (g) where blood is oxygenated. After leaving from the gill, blood enters the pericardial sinus (p) and finally withdrawn into the heart through ostium. Therefore, this is a system constituted of a pump and a controller.

**Figure 2.** Resemblance of a wiring design in CVCSs between evolutionarily distinct two different animals, vertebrates (four chambered) and crustaceans (single chambered). The cardioinhibitory (CI) and cardioacceleratory (CA) nerves, P, pacemaker cells.

### **2. EKG: crustaceans**

notion [2, 3]. We consider that 1/f spectrum is a state where, mathematically, scaling exponent (SI) is 1.0. We have, therefore, made a time series analysis programme in order to check the heartbeat wellness: computing whether or not a time series exhibits SI = 1.0. Our technique is a random-walk analysis, which calculates 'the number of steps proceeded within a box, i.e., increased or decreased' [4, 5]. The name of the method is mDFA (abbreviated name, modified detrended fluctuation analysis). We have explained it elsewhere, about the box, steps and entrance and the exit of a box, and so on [4, 5]. As a result, our method showed that SI can quantify the condition of CVCS [4, 5]. This quantification is like the thermometer. It has a

In particular, as far as we know, the association of high SI with unpredictable cessation of heart pumping has been discovered. It has not been shown empirically before us. We first observed it in the crustacean heart; thereafter, we confirmed the same phenomena (high SI) on humans with ischaemic disease and a person who underwent a surgery that made an inci-

By the way, our heart rhythm is apparently not regular. Cardiac rhythmicity is continuously changing, because CVCS is responding to stimulus from the internal and outer world. Therefore, marked irregularity and/or over-regularity might be a deficient state. At least mDFA seems to detect defect/problem that derives from an injury of the myocardial cells caused by either ischaemic reasons or artificial/synthetic reasons. It seems that mDFA is a better way to compute this correlation between an SI value and a poor condition of

Lower animals such as crustaceans have a heart. Crustacean CVCS has been well studied over 100 years. For example, the English comparative biologist-anatomist Tomas Henry Huxley published about crayfish zoology in ca. 1900s [6]. And Swedish American physiologist Anton Julius Carlson has already documented detailed morphology and physiology of the heart of horseshoe crabs (*Limulus polyphemus*), in 1904 [7]. It is worth noting that Carlson already con-

Until now, the anatomy of cardiac nerve of crustaceans is well documented. The crustacean animal has autonomic nervous system that controls the heart (see Cooper et al., e.g. [8], and legendary articles [9, 10]). Typically, crustacean heart is innervated by two acceleratory nerves and one inhibitory nerve (**Figure 1**, see [11]). **Figure 2** shows a diagrammatical view of cardiac nerves in both vertebrates and crustaceans. Crustacean diagram is based on our publication [11]. In summary, the cardiac inhibitory nerve innervates pacemaker cells (P in **Figure 2**) in both crustaceans and humans. In turn, the cardiac acceleratory nerve innervates not only P cells but also myocardial cells (ventricle cells). As shown in **Figure 2**, it is important to acknowledge that nerve fibres of accelerator (CA) proceed deep inside the heart. This fact presents evidence that CA nerve regulates not only the rhythm of the heart but also the strength of heart contraction. **Figure 2** highlights an important issue in terms of evolution: the heart and its controller system resemble in both invertebrate and vertebrate. Further discussions about the resemblance are shown in Ref. [4]. Thus, we strongly expect that a basic finding obtained from invertebrate animals is applicable to humans, according to an

baseline value. If the body condition is normal, it is 37°.

sidered invertebrate hearts as a model of our heart.

sion of the heart [4, 5].

8 Time Series Analysis and Applications

evolutional view [4].

CVCS.

Therefore, we have been studied crustacean heart as a model of human heart [4, 11, 12]. Crab's electrocardiograms (EKGs) were analysed by a random-walk analysis technique that we innovated by our group [4, 5] and discovered that dying crab hearts (**Figure 3**) show a low scaling exponent [scaling index (SI)], and healthy crab hearts show a normal SI, near 1.0. Experiments on several animal species (crabs, lobsters, isopod Ligia, crayfish and insects) revealed that natural death processes decrease SI, falling towards a low level, that is, SI ≒ 0.5 [4, 5] (**Figure 4**). Then, we encountered strange specimens that exhibited a high SI, such as ~1.5. Their hearts

**Figure 3.** A natural death EKG recorded from a dying coconut crab (*Birgus latro*). From A to F, decrements in scaling exponents. Immediately after F, the heart stops pumping and fibrillation-like electrical signal remained (an arrow).

**Figure 4.** EKG test arena (sea water) and some specimens engaged in the tests. After mounting electrodes, EKGs were continuously recorded for the rest of their life. These specimens were terminally inconvenienced after a period of time, for example, from 2 weeks to 2 years.

stopped suddenly, meaning that they died unpredictably (**Figure 5**): we noticed that high-SI specimens are unique and of rare case. A key observation was that unpredictable death crab always had myocardial injury that was caused by the mounting of artificial EKG electrodes (**Figure 6**).

**Figure 5** shows EKG data taken during the unexpected dying process. We normally put two EKG electrodes into crustacean dorsal carapace. However, this crab (**Figure 6**) received three, an excess electrode. As EKG electrodes have no good contact with the surface of heart muscles, they make EKG signal weak. We never want to damage the heart. However, this insufficient condition sometimes occurred. Any electrode can cause this unwished outcome: damaging local myocardial cells. From this unexpected outcome, we 'accidentally' obtained data that prove that myocardial damage increases SI. Then, we had an idea from this crustacean phenomenon that human ischaemic myocardium damage might be the same in terms of physiological nature, and damaged human heart might be able to be analysed with mDFA (see subsequent text).

Anxiety, Worry and Fear: Quantifying the Mind Using EKG Time Series Analysis http://dx.doi.org/10.5772/intechopen.71041 11

**Figure 5.** Unpredictable death. EKG from a crab (*Portunus* sp.). A similar experiment as shown in **Figure 3**, but this specimen's heart suddenly ceased at an arrow. Note, scaling exponents (SI) are always very high, from A to D.

**Figure 6.** Inside view of a crab carapace. Gazami crab, *Portunus* sp. the approximate size of the heart is shown, pentagonshaped diagram. This picture was taken after the crab's death. Electrode-1, -2, and -3, for EKG. Diameter of electrodes: 1 mm. One can see that electrode-3 is too long in size to damage the heart being located immediately beneath the carapace. Myocardial damage caused unpredictable cessation of heartbeat. It took 2 weeks before this crab stopped her heart pumping, which was unpredictable (see **Figure 5**).

stopped suddenly, meaning that they died unpredictably (**Figure 5**): we noticed that high-SI specimens are unique and of rare case. A key observation was that unpredictable death crab always had myocardial injury that was caused by the mounting of artificial EKG electrodes

**Figure 4.** EKG test arena (sea water) and some specimens engaged in the tests. After mounting electrodes, EKGs were continuously recorded for the rest of their life. These specimens were terminally inconvenienced after a period of time,

**Figure 3.** A natural death EKG recorded from a dying coconut crab (*Birgus latro*). From A to F, decrements in scaling exponents. Immediately after F, the heart stops pumping and fibrillation-like electrical signal remained (an arrow).

**Figure 5** shows EKG data taken during the unexpected dying process. We normally put two EKG electrodes into crustacean dorsal carapace. However, this crab (**Figure 6**) received three, an excess electrode. As EKG electrodes have no good contact with the surface of heart muscles, they make EKG signal weak. We never want to damage the heart. However, this insufficient condition sometimes occurred. Any electrode can cause this unwished outcome: damaging local myocardial cells. From this unexpected outcome, we 'accidentally' obtained data that prove that myocardial damage increases SI. Then, we had an idea from this crustacean phenomenon that human ischaemic myocardium damage might be the same in terms of physiological nature, and

damaged human heart might be able to be analysed with mDFA (see subsequent text).

(**Figure 6**).

for example, from 2 weeks to 2 years.

10 Time Series Analysis and Applications

**Figure 7.** Intermittent-stopping manner of heartbeat. Lobster (*Panulirus japonicus*). The intermittency ceased when a human approached the lobster tank. Note: An increasing tendency of heart rate during the presence of a human (between arrows).

We believed that crustacean heartbeat continuously persists beating, that is, their hearts beat like the human heart does. But it was not the case (**Figure 7**). With EKGs from freely moving lobsters/crabs, we found that the heartbeat pattern is not continuous but intermittent if animals are not disturbed (**Figure 7**). This intermittency is induced by the activity of cardioinhibitory nerve (**Figure 8**, [12]). Then, EKG analysis revealed that a relaxed lobster exhibits an SI near 1.0 and a nervous lobster exhibits an SI near 0.5 (**Figure 9**). These results suggested

**Figure 8.** Simultaneous electro-physiological recording: heart (pacemaker, largest spike size, approximately 3 mV), cardio-regulatory nerve (autonomic impulses, largest spike size, approximately 500 micro-V), and mechanical transducer (myocardial force, the largest peak force of contraction is approximately 1 mg). An increase of a nerve activity corresponds to a complete stop of heartbeat. The smallest spikes in amplitude are the cardio-inhibitory impulses. The other two include the cardio-acceleratory impulses. Hermit crab (*Aniculus aniculus)* (modified from Yazawa and Kuwasawa [12]).

**Figure 9.** A long EKG recording. Lobster, *Panulirus japonicus*. A human visit (thick lines) changes the heartbeat pattern. In relaxed and nervous conditions: SI ≒ 1 and SI ≒ 0.6, respectively (upper inset). SI distinguishes lobster's psychology.

to us that SI might be useful to quantify the psychology of lobster. Indeed, stressful stimuli decrease lobster's SI significantly, and electro-physiologically the nervous/stressful state is a state of acceleration dominant and lost-inhibition controls of the heart (**Figure 7**).

We have long been specifically studying the neurobiology of crustaceans [11]. However, the crustacean experiments opened our eyes bigger, and our viewpoint was extended to human hearts. SI measures could be applicable not only to crustaceans but also to humans at least applying to their time series signal obtained from the heartbeat. According to our guideline, the normal SI ranges approximately 0.8–0.9 < SI < 1.1–1.2 [5].
