Myocardial Perfusion Imaging Study of CO 2 -Induced Panic Attack




Chest pain is often seen alongside with panic attacks. Moreover, panic disorder has been suggested as a risk factor for cardiovascular disease and even a trigger for acute coronary syndrome. Patients with coronary artery disease may have myocardial ischemia in response to mental stress, in which panic attack is a strong component, by an increase in coronary vasomotor tone or sympathetic hyperactivity setting off an increase in myocardial oxygen consumption. Indeed, coronary artery spasm was presumed to be present in cases of cardiac ischemia linked to panic disorder. These findings correlating panic disorder with coronary artery disease lead us to raise questions about the favorable prognosis of chest pain in panic attack. To investigate whether myocardial ischemia is the genesis of chest pain in panic attacks, we developed a myocardial perfusion study through research by myocardial scintigraphy in patients with panic attacks induced in the laboratory by inhalation of 35% carbon dioxide. In conclusion, from the data obtained, some hypotheses are discussed from the viewpoint of endothelial dysfunction and microvascular disease present in mental stress response.


Chest pain is a key symptom in acute coronary syndrome, one of the leading causes of death in the world. Therefore, it requires accurate investigation for rapid identification and early treatment. In contrast, patients at emergency room complaining of chest pain may present symptoms of anxiety and depression with no evidence of acute coronary syndrome. Panic disorder (PD) is a frequent diagnosis in this population. It was found that around 30% of patients experiencing chest pain had PD, 22% of them with no evidence of coronary artery disease (CAD). As part of the multifactorial clinical picture known as mental stress (MS), PD is characterized by the occurrence of panic attacks (PAs), periods of intense fear accompanied by somatic symptoms, described as “respiratory symptoms,” which include choking and/or smothering sensations, shortness of breath, chest pain, and palpitation or accelerated heart rate (HR), all of them possibly present in acute coronary syndrome. Intriguingly, in addition to mimicking CAD, PD has also been identified as a risk factor for ischemic events. Several cases of PA triggering myocardial infarction have been reported. Of interest, acute stress has been linked to myocardial damage even in patients without any evidence of obstructive CAD. The aim of this study is to better assess chest pain present in PA, to exclude the presence of myocardial ischemia. To address this aim, we designed a clinical study in patients with PD and chest pain without known CAD. Here, we describe the preliminary results.


Methods


The present study was approved by the Institutional Ethics Committee, consistent with the terms of Declaration of Helsinki. Written informed consent was obtained from all patients. After testing, all patients were followed at regular outpatient PD treatment at our institution.


The patients met diagnostic criteria for PD after completing a structured interview based on the Diagnostic and Statistical Manual for Mental Disorders. The inclusion criterion was to have a minimum of 4 PAs, at least 1 of which was unanticipated, during the 4 weeks before the initiation of the evaluation. All patients also need to report chest pain, defined as chest pressure, pain, or discomfort, concomitantly with most of attacks. The exclusion criteria were CAD diagnosis, coronary risk factors, and use of cardiovascular, antipsychotic, antidepressant, regular benzodiazepine, or non-benzodiazepine anxiolytic medication.


To rule out myocardial ischemia induced by physical stress, the patients were subjected to a technetium-99m sestamibi single-photon emission computed tomography (sestamibi SPECT) investigation at rest and after maximum performance during a treadmill exercise test. Those with negative ischemic response were invited to undergo a sestamibi SPECT after a carbon dioxide (CO 2 ) panic challenge test. Patients with hypertensive response during treadmill exercise test were also excluded.


The CO 2 panic challenge consisted of 2 sequential vital capacity inhalations of a gas containing 35% CO 2 and 65% oxygen (O 2 ), delivered through a facial mask. Patients with PD are sensitive to small increases in CO 2 , presenting sudden respiratory distress followed promptly by brief hyperventilation and PA similar to the spontaneous presentation that occurs outside the laboratory setting. Immediately after second gas inhalation, technetium-99m sestamibi was injected as a marker of myocardial perfusion, regardless of whether patients presented a PA. SPECT acquisition was performed and independently interpreted by 2 nuclear cardiology specialists.


To record hemodynamic data, they were outfitted with a 12-lead electrocardiograph, a sphygmomanometer, and a pulse oximeter. A catheter was inserted for injection of the radioisotope. Patients rested for 10 minutes in a quiet room, while baseline HR, blood pressure (BP), oxygen saturation (PO 2 ), and electrocardiogram were recorded. After CO 2 challenge, HR, BP, PO 2 , and electrocardiogram were sequentially recorded every 20 seconds for 4 minutes. The double product (DP), the result of multiplying the HR for systolic BP, is a hemodynamic parameter that mirrors the myocardial O 2 consumption and is directly implicated in states of myocardial ischemia. Patients were submitted to specific scales to measure anxiety and panic response before and after the CO 2 challenge.




Results


So far, 7 patients were studied in our lab, 4 women and 3 men, with ages ranging from 25 to 60 years. All had scores >8 in the subsection anxiety of the Hospital Anxiety and Depression Scale and the Mini International Neuropsychiatric Interview (MINI) diagnosis of PD. Only 1 patient had a score >8 for the Hospital Anxiety and Depression Scale for depression, with an MINI diagnosis of major depressive episode. Age, scores in each subscale of Hospital Anxiety and Depression Scale, and MINI diagnosis are described in Table 1 .



Table 1

Age, scores in each subscale of Hospital Anxiety and Depression Scale (HADS), and Mini International Neuropsychiatric Interview (MINI) diagnostic




















































Patient Age (yrs) HADS-A HADS-D MINI
1 60 15 4 PD
2 55 10 1 PD/Ag
3 37 13 4 PD/Ag
4 34 10 11 PD + MDD
5 51 14 5 PD + Ag
6 25 12 6 PD/Ag + PTSD
7 50 15 3 PD/Ag

Ag = agoraphobia; MDD = major depressive disorder; PTSD = posttraumatic stress disorder.


After application of the inhalation test of CO 2 , 57% of patients (4 of 7) showed symptoms and agreed they had a PA. When asked to compare the symptoms after the test with those in spontaneous attacks, 1 patient reported being less intense than the spontaneous, 2 patients reported similar intensity, and 1 patient reported symptoms of greater intensity. Analyzing symptoms presented after CO 2 test, derealization, chest pain, fear of losing control, dizziness, and shortness of breath (hyperventilation) were present in all 4 patients with positive PA. Chest pain was moderate in 2 patients and severe in the other 2 ones. The presence and intensity of symptoms after inhalation of CO 2 are summarized in Table 2 . Although the population studied is not large enough to discuss the results in terms of statistical significance, findings deserve some detailed comments.



Table 2

The presence and intensity of symptoms after inhalation of carbon dioxide (CO 2 )




























































































































Patient Nausea Derealization Paresthesia Waves Chest Pain Fear of Dying Fear of Loosing Control Breathlessness Vertigo Palpitations Tremble Sweating Suffocation
1 0 0 0 0 0 0 0 0 0 0 0 0 2
2 0 2 0 0 2 0 0 0 2 1 0 0 0
3 0 3 0 0 3 4 4 3 4 4 2 0 3
4 0 0 0 0 0 0 0 0 0 0 0 0 0
5 0 3 3 0 3 4 4 3 2 4 3 0 3
6 0 2 0 0 2 0 1 3 2 0 0 0 0
7 0 2 0 0 2 4 4 4 4 0 0 0 4


Neither of the 2 patients who reported palpitations presented significant variations in HR. Tachycardia occurred in only 1 patient, which denied PA. The evolution of BP, both systolic and diastolic, showed no significant changes, except for patient 2 who showed a curve consistent with a hypertensive response after inhalation of CO 2 and consequently the patient was the one who hit the DP of greater value ( Tables 3 and 4 ). None of the 7 patients studied showed ischemic or any other electrocardiographic changes after inhalation of CO 2 .



Table 3

Hemodynamic data of patients after inhalation of carbon dioxide (CO 2 )
























































































































Patient HR SBP DBP
ΔT 0 ΔT 20 seconds ΔT 1 minute ΔT 4 minutes ΔT 0 ΔT 20 seconds ΔT 1 minute ΔT 4 minutes ΔT 0 ΔT 20 seconds ΔT 1 minute ΔT 4 minutes
1 83 87 77 88 130 130 110 130 70 70 70 88
2 78 89 83 77 140 160 190 160 90 90 100 100
3 76 101 79 72 120 120 120 140 80 80 80 90
4 87 107 118 77 130 130 130 140 80 80 80 80
5 81 103 84 69 130 130 130 140 80 80 80 80
6 62 84 69 63 120 110 110 120 80 80 80 80
7 85 97 72 61 110 110 130 100 80 80 80 70

DBP = diastolic blood pressure; SBP = systolic blood pressure.

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Dec 5, 2016 | Posted by in CARDIOLOGY | Comments Off on Myocardial Perfusion Imaging Study of CO 2 -Induced Panic Attack

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