Disaster hypertension and cardiovascular events in disaster and COVID-19 pandemic.

The incidence of large disasters has been increasing worldwide. This has led to a growing interest in disaster medicine. In this review, we report current evidence related to disasters and coronavirus disease-2019 (COVID-19) pandemic, such as cardiovascular diseases during disasters, management of disaster hypertension, and cardiovascular diseases associated with COVID-19. This review summarizes the time course and mechanisms of disaster-related diseases. It also discusses the use of information and communication technology (ICT) as a cardiovascular risk management strategy to prevent cardiovascular events. During the 2011 Great East Japan Earthquake, we used the "Disaster Cardiovascular Prevention" system that was employed for blood pressure (BP) monitoring and risk management using ICT. We introduced an ICT-based BP monitoring device at evacuation centers and shared patients' BP values in the database to support BP management by remote monitoring, which led to improved BP control. Effective use of telemedicine using ICT is important for risk management of cardiovascular diseases during disasters and pandemics in the future.

INTRODUCTION

Many large disasters such as the Great Hanshin‐Awaji Earthquake (1995), the Great East Japan Earthquake (2011), and the Kumamoto Earthquake (2016) have occurred in Japan. As of August 2020, the coronavirus disease‐2019 (COVID‐19) pandemic is still a tense situation because the momentum of infection has not ended and countermeasures are taken worldwide. Anyone may encounter a disaster or pandemic crisis anytime and anywhere. Thus, medical practitioners should be aware of disasters and pandemic‐related diseases. Moreover, the incidence of disaster‐related cardiovascular diseases (CVDs) changes concurrently with time immediately after the occurrence of a disaster.

TIME COURSE AND MECHANISMS OF DISASTER‐RELATED DISEASE

Characteristics of disaster‐related diseases are defined based on the chronological sequence of disease that occurs during and after a disaster. , Activated sympathetic nervous system‐induced diseases such as Takotsubo cardiomyopathy and pulmonary embolism (PE) occur during the first few weeks after a disaster. The risks of sudden death and hypertensive‐related diseases such as stroke, coronary artery disease, and heart failure are approximately doubled after a disaster (Figure 1). The major disaster‐related diseases are listed in Table 1.

FIGURE 1

Time course of the onset of disaster‐related disease. DVT, deep‐vein thrombosis; PTSD, post‐traumatic stress disorder. Source: Kario and colleagues

TABLE 1

Characteristics of disaster‐related CVDs

Disaster‐related cardiovascular diseases	Time of onset	Characteristics
Takotsubo cardiomyopathy	Immediately after the disaster to several weeks	Causes: physical and mental stress, and sympathetic abnormality Risk factors: old age and female sex Comments: benign prognosis if appropriate primary treatment is provided
Dysrhythmia Fatal dysrhythmia Atrial fibrillation		Causes: physical and mental stress, sympathetic abnormality, insomnia Risk factors: presence of arteriosclerosis and high‐risk factors of CVD (old age, smoking habit, HT, diabetes, dyslipidemia, and CKD)
Sudden cardiac death
PE* DVT	1−3 days to several weeks or several months after the disaster *Especially in people living in a shelter, the onset of PE is most often after 1−2 weeks of the disaster	Risk factors: age more than 40 years, female sex, living in a car, comorbidity of trauma, dehydration, poor toilet environment, and living in areas with severe environmental damage
Coronary heart disease Myocardial infarction Unstable angina	Several days to several months or several years after the disaster	Causes: physical and mental stress, sympathetic abnormality, insomnia Risk factors: presence of arteriosclerosis and high risk of CVD (old age, smoking habit, HT, diabetes, dyslipidemia, and CKD), elevated BP (disaster hypertension), dehydration, and lack of usual medications
Stroke Cerebral hemorrhage Cerebral infarct
Heart failure		Causes: physical and mental stress, sympathetic abnormality, insomnia, excess salt intake due to consumption of stored food, and infection (pneumonia) Risk factors: presence of arteriosclerosis and high risk of CVD (old age, smoking habit, HT, diabetes, dyslipidemia, and CKD), elevated BP (disaster hypertension), and irregular intake of usual medications
Disaster hypertension		Causes: physical and mental stress, sympathetic abnormality, insomnia, excess salt intake due to consumption of stored food, and infection (pneumonia)
Respiratory infection	Several days to several months after the disaster	Respiratory infection (pneumonia) may induce CVDs such as heart failure Risk factors: old age and group life in shelters

Abbreviations: BP, blood pressure; CKD, chronic kidney disease; CVD, cardiovascular disease; DVT, deep‐vein thrombosis; HT, hypertension; PE, pulmonary embolism.

After a disaster, people are forced to live in shelters. Physical and mental stresses resulting from changes in the living environment lead to an increase in sympathetic nervous activity, which induces elevation of blood pressure (BP) and a tendency to develop thrombosis. This causes plaque rupture and thrombus formation, resulting in CVD development. , , , , , , , Additionally, sleep disturbances develop over a long period after the disaster. Figure 2 illustrates the mechanism of CVD incidence during a disaster. , , , , , , , ,

FIGURE 2

Potential mechanisms of the disaster‐related cardiovascular risk factors. A disaster induces acute stress and changes in the living environment, which leads to hyperactivity of the sympathetic nervous system. Furthermore, excess salt intake and disruption of the circadian rhythm (eg, sleep disturbances) induce BP elevation or disaster hypertension. In addition to sympathetic hyperactivity, changes in the living environment and lifestyles, such as long stasis and dehydration, cause a tendency for thrombosis. Sympathetic hyperactivity, elevation of BP, and thrombotic tendencies are considered the causes of cardiovascular events. BP, blood pressure; CVD, cardiovascular disease

Takotsubo cardiomyopathy caused by physical and mental stress develops immediately after a disaster. An obvious increase in the incidence of Takotsubo cardiomyopathy was reported after the 2004 Niigata Chuetsu Earthquake compared with its incidence in the previous 3 years. A total of 25 cases were reported within 3 weeks of the disaster, while prior to the disaster, only one case was reported in 2002, 0 in 2003, and one in 4 weeks before the 2004 earthquake. Furthermore, 11 (44%) of the reported cases occurred in older individuals within 6 h after the earthquake, and 24 (96%) of the reported cases occurred in women.

Fatal arrhythmia and sudden cardiac death increase immediately after a disaster. Zhang and colleagues reported that the incidence of fatal ventricular tachyarrhythmia increased in China after the 2008 Wenchuan Earthquake (67 events/10 000 person‐days vs. 7 and 14 events/10 000 person‐days [2 control periods], all p values < .001). Hao and colleagues reported that the incidence of sudden cardiac death increased immediately after the 2011 Great East Japan Earthquake in individuals and areas at risk, which included women, older individuals (>75 years old), and coastal areas severely damaged by tsunami.

The incidence of PE increases from the second to the third day after a disaster. Long‐term rest in a car or shelter, inadequate water intake, and post‐disaster stress promote thrombus formation, resulting in deep‐vein thrombosis (DVT) and PE. Risk factors for DVT include female sex, age >40 years, living in a car, trauma, and toilet environment. Sato and colleagues reported that 178 (10.6%) of 1673 individuals who were screened for DVT using a portable echo 1 month after the 2016 Kumamoto Earthquake had DVT. They indicated the following the risk factors for DVT: age >70 years, daily use of sleeping medications, lower leg edema, and varices in the lower extremities. Moreover, D‐dimer measurement and portable echocardiography are suggested useful for DVT screening.

Hypertension‐related diseases develop immediately after a disaster, and their risk continues until the living environment improves. The elevation of BP immediately after a disaster has been reported. , Disaster hypertension causes various CVDs such as stroke, coronary artery diseases (CADs), and heart failure. , Aoki and colleagues reported that the number of stroke, including cerebral infarction and cerebral hemorrhage, increased immediately after the 2011 Great East Japan Earthquake. Similarly, an increase in the incidence of CADs and aortic dissection was observed. , , The prevalence of CADs was higher 5 years after the 2008 Sichuan Earthquake in China than in other years. An increase in disaster hypertension and arrhythmias such as atrial fibrillation, which is caused by acute stress due to the disaster, may lead to arterial thrombus and plaque rupture in patients at the risk of arteriosclerosis and CVDs.

Subsequently, an increase in the incidence of heart failure during disasters was first reported during the Great East Japan Earthquake. The causes were sympathetic hyperactivity, elevated BP, arrhythmias during the disaster, stagnation of drug procurement, excessive salt intake due to stored food consumption, exposure to cold due to difficulty in controlling room temperature, and pneumonia and other infectious diseases. ,

DISASTER HYPERTENSION: TIME COURSE AND MECHANISM

Disaster hypertension is defined as elevated BP levels (>140/90 mmHg) after a disaster. In Asian patients, BP level is strongly associated with CVD outcomes, and salt sensitivity is strong. , Hence, intensive BP control during a disaster is important for the prevention of CVDs in Asians.

Disaster hypertension occurs immediately after a disaster and continues until both the living environment and lifestyle habits are improved and stabilized. Systolic BP (SBP) has been reported to increase by an average of 5–25 mmHg for 2–4 weeks after an earthquake. , , Large individual differences in the elevation of BP and duration of elevated BP exist. Disaster hypertension is likely to persist for a long period in older patients, in patients with increased salt sensitivity such as those with metabolic syndrome, and in patients with chronic kidney disease, microalbuminuria, and obesity. , , , , ,

The mechanism of disaster hypertension onset includes physical and mental stress due to disasters and changes in the living environment. Disruption of circadian rhythms due to decreased daytime activity and sleep disorders promote sympathetic hyperactivity and increase stress‐induced hormones such as glucocorticoids. , , , Moreover, our research group previously demonstrated that excess salt intake is one of the causes of disaster hypertension in evacuees. We conducted a health survey to monitor BP control in the victims of the 2011 Great East Japan Earthquake who lived in evacuation shelters after the earthquake. We investigated the relationship between salt intake, as estimated by the spot urine method, and the presence of disaster hypertension in 272 evacuees. In this study, disaster hypertension, defined as an SBP of ≥140 mmHg or a diastolic BP of ≥90 mmHg as measured using an automatic BP monitoring device at an evacuation center, was found in 58% of the participants, and its prevalence increased by 16% for each 1‐g increase in estimated salt intake. The odds ratio (95% confidence interval) for developing disaster hypertension per 1‐g increase in estimated salt intake in participants without a diagnosis of hypertension before the earthquake and with a high risk of salt sensitivity (age ≥65 years and presence of obesity, chronic kidney disease, and diabetes) was 1.46 (1.19–1.79). These findings suggest that increased salt intake and high salt sensitivity may be important mechanisms for the development of disaster hypertension. Although there is still a lack of robust evidence regarding the mechanism of disaster hypertension, preventive measures may be important to maintain the circadian rhythm by improving the living environment and sleep quality and maintaining physical activity during a disaster as well as to reduce salt intake in high‐risk patients. , , , , ,

MANAGEMENT OF DISASTER HYPERTENSION AND DISASTER‐RELATED CVDS

The flow chart of disaster hypertension management is presented in Figure 3. , First, as regards BP evaluation, an increase in the whitecoat effect is observed during a disaster. Therefore, we recommend the evaluation of self‐BP measurements (out‐of‐office BP) along with that of BP values measured by the relief team and medical institutions (office BP). An automatic BP monitoring device should be installed in evacuation centers for self‐BP measurements.

FIGURE 3

Flow chart of disaster hypertension management. BP, blood pressure

Second, no clear evidence is available regarding the target BP level during a disaster. However, we recommend that the primary target BP level should be an office BP of less than 140/90 mmHg in the acute phase of the disaster because the diagnostic criteria for disaster hypertension are a BP of ≥140/90 mmHg. , Once the living environment improves, the target BP level should be an office BP of less than 130/80 mmHg based on most international guidelines. , With regard to the use of antihypertensive medications during disasters, pre‐disaster medications should be continued if possible. In addition, we recommend the use of long‐acting calcium channel blockers (CCBs) at the beginning of the treatment for disaster hypertension or when BP control is poor during a disaster. The BP‐lowering effect of long‐acting CCBs depends on the BP level upon administration. The higher the BP, the lower the BP; however, if the BP is relatively low, it may not be lowered further. Alternatively, long‐acting CCBs are considered suitable for disaster hypertension because of the reliable reduction in BP levels and BP variability.

The authors developed an assessment and prevention score for disaster‐related CVDs (Disaster Cardiovascular Prevention [DCAP] risk/prevention score) based on the characteristics of the disaster‐related disease and risk factors. The DCAP score consists of a risk score (AFHCHDC7) and a prevention score (SEDWITMP8) (Figure 4). We asked the medical volunteer teams to use this score to prevent disaster‐related CVDs during the Great East Japan Earthquake. , Individuals with a risk score of ≥4 points were categorized into the high‐risk group. Individuals in the high‐risk group should attempt to improve their living environment and lifestyle to achieve a prevention score of ≥6 points. , , ,

FIGURE 4

Disaster cardiovascular prevention risk score (AFHCHDC7) and prevention score (SEDWITMP8). *Total number of risk factors as an individual's risk score (0–7 points). #Total number of prevention factors as an individual's prevention score (0–8 points). The target prevention score was ≥6 particularly in high‐risk patients. DCAP, disaster cardiovascular prevention; SBP, systolic blood pressure. Source: Kario and colleagues

During the Great East Japan Earthquake, we used the DCAP system that was used for BP monitoring and risk management using information and communication technology (ICT). In cooperation with the practitioners in Minamisanriku Town, where the damage due to the earthquake was serious, we introduced an ICT‐based BP monitoring device at evacuation centers and shared patients’ BP values in the database to support BP management by remote monitoring (Figure 5). , , Consequently, we succeeded in improving BP control and suppressing seasonal variation in BP (ie, an increase in BP from summer to winter), which has been reported over the years. , Thus, we believe that ICT might be useful for anticipating needed interventions against BP elevation after a disaster and may contribute to the suppression of disaster‐related CVDs. Moreover, patients living in the disaster area may have difficulty visiting medical facilities. Recently, these ICTs have made it possible for home BP monitoring and medical consultation in telemedicine. Thus, by using ICT to manage high‐risk patients closely, we can reduce the burden on medical institutions in disaster areas and support efficient risk management. , In the future, ICT is expected to be a cooperation system that connects temporary housing and regional medical institutions in disaster areas.

FIGURE 5

Disaster cardiovascular prevention network. The DCAP network system uses a blood pressure (BP) monitoring device equipped with a card reader and information and communication technology to measure BP and sends the measured BP values to a cloud data center. This BP monitoring device can be used for home BP monitoring. The DCAP network system can be useful for the prevention of cardiovascular events in high‐risk patients living in evacuation centers or their houses during a disaster. DCAP, disaster cardiovascular prevention. Source: JCS, JSH, and JCC Joint Working Group, Kario and colleagues

COVID‐19 PANDEMIC AND CVD

COVID‐19 is currently a pandemic because of its explosive infectivity. Patients with CVD comorbidities have a higher risk for severe COVID‐19 infection. Furthermore, COVID‐19 infection may cause abnormal coagulation and myocardial injury due to acute inflammation and may be associated with CVDs. ,

Patients with hypertension may have a poor prognosis after COVID‐19 infection. An epidemiological study in Italy reported that the mean age of the 3200 patients who died of COVID‐19 was 78.5 years, of which 98.7% had one or more comorbidities, 74% had hypertension, and 52% used renin–angiotensin system (RAS) inhibitors. However, the results of these observational studies could not be confirmed by direct evidence because of many confounding factors such as age and because hypertension is a risk factor for poor prognoses such as severe illness and death. It is reasonable to conclude that older COVID‐19 patients and general risk factors of CVD are at risk for severe morbidity and mortality. ,

As a mechanism to enter and infect cells, the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) binds to the transmembrane of angiotensin‐converting enzyme 2 (ACE2), indicating that high ACE2 expression is susceptible to infection with SARS‐CoV‐2. Additionally, pathways related to ACE on the cell membrane affect inflammatory cytokines, which represent potential mechanisms for the cytokine storm seen in patients with COVID‐19. Therefore, there is a concern that RAS inhibitors may increase the incidence and mortality of COVID‐19 because RAS inhibitors have been shown to increase the expression of ACE2 on cell membranes. However, observational studies from several countries have reported that the use of RAS inhibitors is not related to the incidence and severity of COVID‐19 infection. , , Additionally, a recent observational study reported that RAS inhibitors could be beneficial for the prevention of disturbance of consciousness. At the time of writing this paper, no robust evidence confirmed that RAS inhibitors increase the risk of infection and mortality of COVID‐19. Many societies and experts in Japan and other countries have announced that RAS inhibitors should not be discontinued in patients with hypertension or heart failure due to fear of COVID‐19 infection. ,

In severe COVID‐19 infection, in addition to the severe respiratory syndrome, thrombotic tendency, and myocardial injuries develop, which may lead to arterial or venous thrombosis and heart failure. Further, an observational study reported that anticoagulation therapy was associated with improved outcomes during hospitalization. Moreover, some observational studies have reported that the levels of some biomarkers related to myocardial injury and thrombosis, such as troponin and D‐dimer, are elevated in COVID‐19 patients. , , In severe cases, evaluation of biomarkers related to myocardial injury and of lung lesions is necessary to stratify the risk of CVD complications and organ damage. Table 2 summarizes the points of evaluation and management of CVDs related to COVID‐19, which are described in this section. , , , , , , , , , , , Besides, the COVID‐19 pandemic has brought great changes in people’s lifestyles. The number of outpatients who directly visit a medical institution decreases due to restrictions on going outdoors. To solve this problem, telemedicine using ICT would be useful in outpatient practice.

TABLE 2

COVID‐19 and comorbidities of CVD: assessment and management

Patients with hypertension, especially older individuals and those with other known risk factors, are at an increased risk of developing severe symptoms during COVID‐19 infection

High‐risk patients with CVDs, such as those with hypertension, are more likely to develop cardiac injury during COVID‐19 infection. Particularly, in these high‐risk patients, several biomarkers such as troponin and D‐dimer should be assessed along with respiratory symptoms to evaluate organ injury including myocardial injury In hospitalized COVID‐19 patients, cardiac injury, which was evaluated by high‐sensitivity troponin and creatinine kinase‐myocardial band, was associated with a higher risk of in‐hospital mortality

Anticoagulation therapy may be effective for improving the prognosis in COVID‐19 patients who require treatment with as well as without respiratory ventilation An observational study reported that anticoagulation therapy was associated with improved prognosis during hospitalization 33

In patients with diabetes, myocardial injury and arteriovenous thrombosis should be carefully evaluated

Oxygen saturation should be determined at presentation; if oxygen saturation is <94%, then COVID‐19 should be considered severe

Antihypertensive therapy with ACE inhibitors or ARBs in COVID‐19 patients should be continued with careful monitoring of hypertension and kidney injury Use of ACE inhibitors or ARBs does not increase the incidence of hospitalization or mortality compared with other classes of antihypertensive medications Unmedicated older COVID‐19 patients whose only comorbidity is hypertension can be treated with calcium channel blockers

Medical practitioners should be aware of physical manifestations of stress (eg, cardiovascular events), even in individuals without COVID‐19 (especially those with pre‐existing hypertension)

Even after recovery from COVID‐19, the existence of myocardial injury should be considered In hospitalized COVID‐19 patients, cardiac injury, which was evaluated by high‐sensitivity troponin and creatinine kinase‐myocardial band, was associated with a higher risk of in‐hospital mortality.An observational study using cardiac MRI revealed that patients who had recovered from COVID‐19 infection had abnormal findings 36

Medical practitioners working on treatment of COVID‐19 should be checked for their mental state and psychological distress. Moreover, general people, that is, non‐medical health care workers, also need to be checked for psychological distress in the era of COVID‐19 37

Abbreviations: ACE, angiotensin‐converting enzyme; ARB, angiotensin receptor blocker; COVID, coronavirus disease; CVD, cardiovascular disease; MRI, magnetic resonance imaging.

An observational study reported that anticoagulation therapy was associated with improved prognosis during hospitalization

In hospitalized COVID‐19 patients, cardiac injury, which was evaluated by high‐sensitivity troponin and creatinine kinase‐myocardial band, was associated with a higher risk of in‐hospital mortality.An observational study using cardiac MRI revealed that patients who had recovered from COVID‐19 infection had abnormal findings

DISRUPTION OF HEALTH CARE SYSTEMS

In the event of a disaster, health care systems are disrupted. Even routine care preventing new CVD or control of pre‐existing CVD may be affected. Many countries and regions differ in health care resilience due to available resources and the degree of preparedness. Medical provider groups will need to adjust their usual practice and mobilize resources to manage a disaster situation quickly. This may mean that elective clinical work, research, and academic duties are deferred, and resources are pushed toward direct medical care in the affected disaster area.

CONCLUSIONS

Recently, interest in medical care during disasters has been increasing owing to the occurrence of many large natural disasters worldwide. New findings on disaster‐related CVDs and disaster hypertension are being reported, and their preventive and coping methods are being developed. Moreover, in the future, the effective use of telemedicine using ICT would be important for risk management of CVDs during disasters and pandemics. , , ,

CONFLICT OF INTEREST

J Shin received lecture honoraria from Pfizer Inc, Hanmi Pharm. Co. Ltd., Yuhan Co. Ltd., Boryung Pharmaceutical Co. Ltd., and consulting fees from Hanmi Pharm. Co. Ltd. Handok Kalos Medical Inc, and research grants from Sanofi Pharm. and Hanmi Pharm. Co. Ltd. Siddique has received honoraria from Bayer, Novartis, Pfizer, ICI, and Servier, and travel, accommodation, and conference registration support from Hilton Pharma, Atco Pharmaceutical, Highnoon Laboratories, Horizon Pharma, and ICI. YC Chia has received speaker honoraria and sponsorship to attend conferences and seminars from Boeringher‐Ingelheim, Pfizer, Omron, Servier, and Xepa‐Sol and investigator‐initiated research grants from Pfizer and Omron. CH Chen reports personal fees from Novartis, Sanofi, Daiichi Sankyo, SERVIER, Bayer, and Boehringer Ingelheim Pharmaceuticals, Inc HM Cheng received speaker honoraria and sponsorship to attend conferences and CME seminars from Eli Lilly and AstraZeneca; Pfizer Inc; Bayer AG; Boehringer Ingelheim Pharmaceuticals, Inc; Daiichi Sankyo, Novartis Pharmaceuticals, Inc; SERVIER; Co., Pharmaceuticals Corporation; Sanofi; TAKEDA Pharmaceuticals International; Menarini Co., Ltd., and served as an advisor or consultant for ApoDx Technology, Inc JG Wang has received research grants from Chendu Di‐Ao and Omron, and lecture and consulting fees from AstraZeneca, Novartis, Omron, Servier, and Takeda. K Kario reports receiving research grants from A&D Co. and Omron Healthcare. Other authors report no potential conflicts of interest related to this review.

AUTHORS’ CONTRIBUTION

Kario K takes primary responsibility for this paper. Narita K wrote the manuscript. Narita K, Hoshide S, Tsoi K, Siddique S, Shin J, Chia YC, Tay JC, Teo BW, Turana Y, Chen CH, Cheng HM, Sogunuru GP, Wang TD, Wang JG, and Kario K reviewed/edited the manuscript.