Mental Health Status in Patients Undergoing Intracoronary Acetylcholine Provocation Test.

BACKGROUND: Previous studies showed the relation of mental distress such as anxiety and depression to coronary vasoconstriction and myocardial ischemia. However, the mental health status of patients suspected to have vasospastic angina is unclear. METHODS: A total of 99 patients underwent intracoronary acetylcholine (ACh) provocation tests for the diagnosis of vasospastic angina and mental health assessment using the 12-item General Health Questionnaire (GHQ-12) and State-Trait Anxiety Inventory Form Y (STAI Y-2). Patients with binary GHQ-12 ≥ 4 were defined as having poor mental health. RESULTS: Median GHQ-12 and STAI Y-2 were 3 [1, 6] and 44 [36, 50]. Forty-one (41%) patients had binary GHQ-12 ≥ 4, and 48 (48%) had positive ACh provocation tests. The number of provoked vasospasms and rate of electrocardiographic change and chest pain during ACh tests were not significantly different between patients with and without GHQ-12 ≥ 4. The incidence of positive ACh provocation test was similar between the two groups (49% vs. 48%, p = 1.00). The multivariable analysis indicated that younger age, no history of percutaneous coronary intervention and no diabetes mellitus were factors associated with higher GHQ-12 and/or STAI Y-2 scores. CONCLUSIONS: More than 40% of patients who underwent ACh provocation tests had poor mental condition. No impact of mental distress on positive ACh tests was found in this study.

Neurocognition in treatment-resistant hypertension: profile and associations with cardiovascular biomarkers.

BACKGROUND: Hypertension in midlife has been associated with increased risk of stroke and neurocognitive decline. Few studies, however, have examined neurocognition among individuals with treatment-resistant hypertension or potential mechanisms by which treatment-resistant hypertension may impair neurocognition. METHODS: We examined the pattern of neurocognitive impairment and potential mechanisms in a sample of 96 overweight adults with treatment-resistant hypertension, aged 41-81 years. Neurocognitive function was assessed using a 45-min test battery consisting of executive function and memory. Vascular and metabolic mechanisms examined included cerebrovascular risk factors (CVRFs: Framingham Stroke Risk Profile), insulin sensitivity (homeostatic model assessment of insulin resistance), waist-to-hip ratio, microvascular function (hyperemic response), and peak oxygen consumption from an exercise treadmill test. Simple path analyses were used to assess the association between potential vascular and metabolic mechanisms and neurocognition. RESULTS: Neurocognitive impairments were common, with 70% of the sample exhibiting impaired performance on at least one executive function subtest and 38% on at least one measure of memory. Higher levels of aerobic fitness, greater insulin sensitivity, and better microvascular function, as well as lower CVRFs and waist-to-hip ratio were associated with better neurocognition. In path analyses, aerobic fitness, microvascular function, and CVRFs all were independently associated with neurocognitive performance. Insulin resistance associated with worse executive function but better memory performance among older participants. CONCLUSION: Neurocognitive impairments are common in adults with treatment-resistant hypertension, particularly on tests of executive function. Better neurocognition is independently associated with aerobic fitness, microvascular function, and CVRFs.

Prevalence of treatment-resistant hypertension and important associated factors-results from the Swedish Primary Care Cardiovascular Database.

We aimed to describe the prevalence, treatment, and associated comorbidity of treatment-resistant hypertension (TRH). This registry-based cohort study from The Swedish Primary Care Cardiovascular Database assessed 53,090 hypertensive patients attending primary care. Patients adherent to antihypertensive treatment measured by pharmacy fills and with proportion of days covered ≥80% were included. The prevalence of TRH was 17% when considering all current TRH definitions. Adherence to mineralocorticoid receptor antagonists differed between TRH- and non-TRH patients (8 vs. 4%). Higher frequencies (prevalence ratio and 95% confidence intervals) of diabetes mellitus (1.59, 1.53-1.66), heart failure (1.55, 1.48-1.64), atrial fibrillation (1.33, 1.27-1.40), ischemic heart disease (1.25, 1.20-1.30), and chronic kidney disease (1.38, 1.23-1.54) were seen in patients with TRH compared to patients without TRH. These findings, in a population with valid data on medication adherence, emphasize a broad preventive approach for these high-risk patients.

A practical approach for measurement of antihypertensive medication adherence in patients with resistant hypertension.

Confirmation of medication adherence is a challenge in clinical practice and essential for the accurate diagnosis of resistant hypertension. Although it is well established that drug adherence is critical for controlling blood pressure, there are still difficulties applying a simple, inexpensive, and reliable assessment of adherence in the clinical setting. We aimed to test a simple method to assess adherence in resistant hypertensive (RH) patients. A pilot study with normotensives or mild/moderate hypertensive subjects was performed to provide a fluorescence cutoff point for adherence. After that, 21 patients referred to the Resistant Hypertension Clinic had triamterene prescribed and were monitored for a 30-day period. We conducted two unannounced randomly selected home visits for urine collection to test drug intake that day. Office, home and 24-hour ambulatory blood pressure, biochemical data, and the 8-item Morisky Medication Adherence Scale (MMAS-8) were systematically acquired. According to adherence indicated by urine fluorescence, subjects were divided into adherent and nonadherent groups. We found 57% of nonadherence. No differences were found between groups regarding baseline characteristics or prescribed medications; Kappa's test showed concordance between adherence through MMAS-8 items and fluorescence (kappa = 0.61; 95% confidence interval: 0.28-0.94; P = .005). Nonadherent patients had higher office (81 ± 11 vs. 73 ± 6 mm Hg, P = .03), 24-hour ambulatory blood pressure monitoring (75 ± 9 vs. 66 ± 7 mm Hg, P = .01), and home blood pressure measurement (77 ± 9 vs. 67 ± 8 mm Hg, P = .01) diastolic blood pressure than their counterparts. Nonadherence to antihypertensive therapy is high in patients with RH, even when assessed in clinics specialized in this condition. Fluorometry to detect a drug in the urine of RH patients is safe, easy, and reliable method to assess adherence.

Anxiety score as a risk factor for radial artery vasospasm during radial interventions: a pilot study.

We determined the role of anxiety level on radial artery spasm during transradial coronary angiography. Eighty-one patients who had an indication for coronary angiography were enrolled. Radial artery vasospasm was determined by addressing 5 signs: persistent forearm pain, pain response to catheter manipulation, pain response to sheath withdrawal, difficult catheter manipulation after being "trapped" by the radial artery, and considerable resistance on withdrawal of sheath. Radial spasm defined as at least 2 of the 5 signs. The Hamilton Anxiety scale questionnaire was used to determine the level of anxiety. Vasospasm was observed in 19.1% of the patients. Anxiety score was significantly higher in women (11.1 ± 7.2 vs 17.6 ± 7.3; P < .001). Vasospasm was significantly correlated with female sex (P < .001, r = .43) and anxiety score (P = .007, r = .29). Female sex was associated with higher anxiety scores (P < .001, r = .43). In conclusion, higher anxiety scores and female sex are important risk factors for radial artery vasospasm.

Killer dreams.

Emotional stress is a recognized trigger for coronary artery spasm. An association between dreams and sudden death is described in folklore and medical history, and originates from the common experience of being awakened by vivid, frightening dreams, with racing pulse, cold sweats and other physiological responses associated with intense distress. Intense alterations in autonomic activity during dreaming can have dire consequences in patients with cardiovascular disease. Four patients with no evidence of underlying coronary artery disease, where emotional stress produced by nightmares or 'deadly dreams' caused coronary artery dissection in two and vasospasm in the other two, leading to life-threatening cardiac events, are presented. A possible mechanism is speculated.

A psychobehavioral factor, alexithymia, is related to coronary spasm.

The aim of this study was to assess whether the psychobehavioral pattern alexithymia is related to coronary artery spasm. Alexithymia, deficient psychological awareness, was examined using the Minnesota Multiphasic Personality Inventory Alexithymia Scale in 100 patients with angina pectoris in whom coronary spasm, defined as > or = 99% coronary narrowing, was documented upon ergonovine provocation, and in 109 patients with chest pain syndrome who were shown to have almost normal coronaries without inducible coronary spasm on coronary angiogram (control group). Alexithymia was approximately twice as prevalent in the coronary spasm group (31%) as in the control group (14%) (p<0.01). Among various conventional risk factors including hyperlipidemia, obesity, diabetes mellitus, hypertension, hyperuricemia, or family history of ischemic heart disease, only male sex and smoking were more prevalent in the coronary spasm group than in the control group (p<0.001). The odds ratios of coronary spasm adjusted for all the other risk parameters including sex and age were 4.14 [95% confidence interval (CI) 1.81-9.47] for alexithymia and 2.38 (95, CI 1.18-4.82) for smoking. A psychobehavioral pattern, alexithymia, relates to coronary spasm. This relationship is independent of the conventional coronary risk factors.

Prinzmetal's angina and emotions: A neglected psychosomatic entity.

Prinzmetal's angina, a form of angina precipitated by vasoconstriction or spasm, appears to be a somatic phenomenon, but there is evidence, from research and case reports, of a major psychological component. In this study, individuals with Prinzmetal's angina were interviewed to determine the nature of their interpersonal relationships and their intrapsychic state at the time of onset of their chest pain. In addition, short developmental histories were obtained. The authors found that onset of chest pain was related to experiencing intense affect, and multiple levels of interpersonal and intrapsychic conflict, with strong conscious and unconscious, emotional and ideational links to previous traumas.

Psychosocial factors impair vascular responses of coronary arteries.

BACKGROUND: Four sets of monkeys were used to examine the effect of chronic psychosocial disruption and diet on dilator responses of coronary arteries. METHODS AND RESULTS: One set consisted of monkeys consuming monkey chow and living in a stable social setting (nonatherosclerotic controls, n = 6). Three sets consumed an atherogenic diet for 14 months followed by one of three treatments for the next 16 months: 1) a high-cholesterol diet and housed in unstable social groups (n = 9); 2) a low-cholesterol diet and housed in unstable (n = 8); or 3) stable groups (n = 10). Quantitative coronary angiography revealed that intracoronary infusion of acetylcholine resulted in a change of diameter (versus infusion of 5% dextrose in water) of +4 +/- 1% in control monkeys and -11 +/- 4% in unstable monkeys consuming a high-cholesterol diet (p less than 0.05). In monkeys consuming the cholesterol-lowering diet, the change in artery diameter was +2 +/- 4% in stable and -10 +/- 4% in unstable social conditions (p less than 0.05) despite a similar plaque size (0.4 +/- 0.2 and 0.5 +/- 0.1 mm2) and total plasma cholesterol concentrations (179 +/- 9 and 172 +/- 6 mg/dl), respectively. The arterial response to nitroglycerin was similar among all groups of monkeys. CONCLUSIONS: We conclude that chronic social disruption is associated with relative arterial constriction in response to acetylcholine in atherosclerotic monkeys consuming a cholesterol-lowering diet.

Microvascular angina and panic disorder.

Recent cardiac studies have suggested that patients with chest pain and angiographically normal coronaries have "microvascular angina" (MVA). In contrast, prior psychiatric studies have shown that some of these patients have panic disorder (PD). We compared the clinical and psychologic characteristics of fifteen patients with MVA and fifteen patients with panic disorder (PD), and examined response to lactate infusion in a subgroup of MVA patients. Although 40 percent of MVA patients met criteria for PD and had chest pain following lactate infusion, there were psychologic and symptomatic differences between the MVA and PD groups. These results reflect either co-morbidity of MVA and PD in some patients or two types of MVA, one of primary cardiac origin and one a centrally mediated epiphenomenon of the increased autonomic arousal seen in PD.

Physiopathological considerations on the arterial coronary spasm. Some diagnostic and therapeutical conclusions.

Starting from the cyclicity of the anginal attack in variant angina, the authors point out the role of alkalosis, besides the richness in alfa-adrenoceptors of the great coronary trunks. At the level of the muscular cell there is a competition between H+-ions and Ca++-ions. The diminution of H+-ions as a result of alkalosis brings about the penetration of Ca++ into the cell and the appearance of the coronary spasm. So, we worked out an original method for the provocation of the spasm (the cold and hiperpneea test) and an original therapeutical procedure (by acetozolamid). We present, herein the first results scored in 16 patients.

Coronary vasospasm: a neuro-behavioral event?

Evidence exists for the presence of a neuro-anatomy that can produce cardiac vasospasm. Recent experimental and clinical data suggest that this neuro-anatomic mechanism can be activated by behavioral events in the psycho-social surround of the patient with coronary artery disease. I hypothesize that this mechanism can produce myocardial ischemia and can explain the variability in onset of clinical angina.

[Relation between personality and spastic angina]. / Relations entre personnalité et angor spastique.

The personalities of 60 patients suffering from episodes of retrosternal pain were evaluated by means of psychological tests ( Cattel 's questionnaire and Eysenck's personality inventory) and semi-directive interviews. The patients fell into three groups: group I patients (n = 21) had atheromatous lesions of the coronary arteries detected at angiography; group II patients (n = 19) had normal or subnormal coronary arteries, but angiography demonstrated arterial spasm; group III patients (n = 20) had angiographically normal coronary arteries without spasm. A statistically significant difference (p less than 0.05) was noted between groups I and II, but not between groups II and III. Eleven of the 21 patients in group I presented with an obsessional personality which was not found in groups II and III where 13/19 and 16/20 patients respectively had a hysterical personality.