Anxiety Disorders, Hypertension, and Cardiovascular Risk: A Review

Abstract

Hypertension, coronary heart disease (CHD), and anxiety disorders all cause substantial morbidity to patients and costs to the healthcare system. Associations between these diseases have been hypothesized and studied for decades. In particular, psychosocial stressors associated with anxiety disorders raise autonomic arousal via the hypothalamic-pituitary axis which increases circulating catecholamines. This heightened arousal is associated with an increased risk of hypertension and a pro-inflammatory state and, consequently, development of coronary heart disease. This association holds across the spectrum of anxiety disorders (generalized anxiety, posttraumatic stress disorder, panic disorder, and obsessive compulsive disorder) and also when controlling for comorbid conditions such as depression and physical ailments. Multiple cross sectional studies reveal a positive association between anxiety and hypertension. These associations are bidirectional, with those with hypertension being more likely to have anxiety and those with anxiety being more likely to have hypertension. However, a few studies have shown no association. Longitudinal studies point to an increased risk of development of hypertension in patients who suffer from anxiety. More convincing studies show links between anxiety symptoms and disorders, including panic disorder and PTSD, and cardiovascular outcomes. Drawing broad conclusions from these studies is challenging, however, given the multiplicity of scales used to measure anxiety disorders. Anxiety, hypertension, and CHD are common conditions seen in primary care, and anxiety may be an important predictor of future CHD outcomes. Better recognition of the association of these conditions and the possible roles of each in development of the other should alert primary care providers to be vigilant in monitoring and treating anxiety, hypertension, and CHD.

Long-term follow-up of psychosocial distress after early onset preeclampsia: the Preeclampsia Risk EValuation in FEMales cohort study

“…Hypertension is part of a cardiovascular risk profile. Significant bidirectional associations between hypertension and psychosocial risk factors have been observed, although there is considerable heterogeneity between different studies, and an absence of associations has been observed as well [30][31][32]. Overall, the present findings do not confirm a strong effect of hypertension as part of a cardiac risk profile, on the association between PE and long-term psychosocial distress.…”

Non-pharmacological strategies to decrease anxiety in cardiac catheterization: integrative review

“…Anxiety is characterized by symptoms such as palpitations, sweating, trembling or shaking, shortness of breath or smothering sensations, chest pain or discomfort, and/or stomach distress (6) . Anxiety activates the sympathetic nervous system leading to a variety of physiological responses (7) , such as tachycardia, sweating, increased oxygen consumption, hypertension, which can worsen the evolution of the patient. In addition, anxiety can have a negative effect on a patient's clinical outcomes such as treatment refusal and reduced tolerance to pain before, during and after the catheterization intervention.…”

Anksioznost in koronarna bolezen srca

“…Te spremembe pa vodijo do tromboze koronarnih arterij prek hemodinamskih učinkov na aterosklerotične plake ali aktiviranja protrombogenih faktorjev in de novo tromboze (47). Aktivirata živčno-hormonski sistem, hipotalamično-hipofizno-adrenalno os (HHA-os) in simpatični živč-ni sistem, ki imata sistemske in lokalne učinke (47)(48)(49). Zaradi vazokonstrikcije se poviša krvni pritisk, pospeši se prevajanje iz sinusnega vozla in poviša frekvenca srca (47)(48)(49).…”

“…Aktivirata živčno-hormonski sistem, hipotalamično-hipofizno-adrenalno os (HHA-os) in simpatični živč-ni sistem, ki imata sistemske in lokalne učinke (47)(48)(49). Zaradi vazokonstrikcije se poviša krvni pritisk, pospeši se prevajanje iz sinusnega vozla in poviša frekvenca srca (47)(48)(49). Ob tem se poveča delo in poraba kisika v srčni mišici, kar lahko vodi do raztrganosti plaka (47)(48)(49).…”

“…Zaradi vazokonstrikcije se poviša krvni pritisk, pospeši se prevajanje iz sinusnega vozla in poviša frekvenca srca (47)(48)(49). Ob tem se poveča delo in poraba kisika v srčni mišici, kar lahko vodi do raztrganosti plaka (47)(48)(49). Delovanje parasimpatičnega živčevja se ob tem zmanjša, zato se zmanjša tudi variabilnost srčne frekvence, ki je znan dejavnik tveganja za kardiovaskularno obolevnost in smrtnost (47).…”