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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients under evaluation for cardiac transplant surgery were seen for routine psychiatric diagnosis and treatment. Of 35 patients with idiopathic cardiomyopathy, 83% (N = 29) had definite or probable panic disorder. Of 25 patients with postinfarction cardiac failure, rheumatic heart disease, or congenital heart disease, only 16% (N = 4) had definite or probable panic disorder. The authors suggest that autonomic mechanisms may underlie the association of cardiomyopathy and panic disorder and that increased cardiac sympathetic tone or circulating catecholamines may cause myocarditis and cardiomyopathy.
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PMID:Idiopathic cardiomyopathy and panic disorder: clinical association in cardiac transplant candidates. 331 Jun 71

Regional sympathetic activity can be studied in humans using electrophysiological methods measuring sympathetic nerve firing rates and neurochemical techniques providing quantification of noradrenaline spillover to plasma from sympathetic nerves in individual organs. Essential hypertension: Such measurements in patients with essential hypertension disclose activation of the sympathetic outflows to skeletal muscle blood vessels, the heart and kidneys, particularly in younger patients. This sympathetic activation, in addition to underpinning the blood pressure elevation, most likely also contributes to left ventricular hypertrophy, and to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidaemia. Antihypertensive drugs, such as moxonidine, which act primarily by inhibiting the sympathetic nervous system, should have additional clinical benefits beyond those attributable to blood pressure reduction, in protecting against hypertensive complications. Obesity-related hypertension: Understanding the neural pathophysiology of hypertension in the obese has been difficult. In normotensive obesity, renal sympathetic tone is doubled, but cardiac noradrenaline spillover (a measure of sympathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal noradrenaline spillover, but without suppression of cardiac sympathetics (cardiac sympathetic activity being more than double that of normotensive obese and 25% higher than in healthy volunteers). Increased renal sympathetic activity in obesity may be a 'necessary' cause for the development of hypertension (and predisposes to hypertension development), but apparently is not a 'sufficient' cause. The discriminating feature of the obese who develop hypertension is the absence of the adaptive suppression of cardiac sympathetic tone seen in the normotensive obese. Heart failure: In cardiac failure, the sympathetic nerves of the heart are preferentially stimulated. Noradrenaline release from the failing heart at rest in untreated patients is increased as much as 50-fold, similar to the level seen in the healthy heart during near-maximal exercise. Activation of the cardiac sympathetic outflow provides adrenergic support to the failing myocardium, but at a cost of arrhythmia development and progressive myocardial deterioration. Psychosomatic heart disease: No more than 50% of clinical coronary heart disease is explicable in terms of classical cardiac risk factors. There is gathering evidence that psychological abnormalities, particularly depressive illness, anxiety states, including panic disorder and mental stress, are involved here, 'triggering' clinical cardiovascular events, and possibly also contributing to atherosclerosis development. The mechanisms of increased cardiac risk attributable to mental stress and psychiatric illness are not entirely clear, but activation of the sympathetic nervous system seems to be of prime importance.
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PMID:Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease. 1134 14

Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
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PMID:Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder. 1524 Apr 8

We report a case of serotonin syndrome that occurred in a patient with chronic heart failure associated with a panic disorder. The 39-year-old Japanese man had been treated with paroxetine at 20 mg/d for 1 1/2 years. He presented with rhabdomyolysis, renal failure, fulminant liver failure, cardiac conduction disturbance, and disseminated intravascular coagulation, as well as conventional symptoms of serotonin syndrome including alterations in cognition (disorientation, confusion) and behavior (restlessness), autonomic nervous system dysfunction (fever, shivering), and abnormal neuromuscular activity (ataxia, hyperreflexia, myoclonus). All medications prescribed before hospital admission were discontinued. After 24 hours of continuous venovenous hemofiltration, diuresis resumed and renal and liver function improved rapidly. Disorientation, restlessness, hyperreflexia, and myoclonus abated slowly over the next 72 hours. The patient's anxiety subsided more slowly, and he recovered completely 1 week later. The plasma concentration of paroxetine was elevated far above the upper limit of the therapeutic range. The patient had cytochrome P-450 (CYP) 2D6*1/*5, a heterozygosity of an inactivated allele of CYP2D6, which metabolizes paroxetine. The patient was determined to be an intermediate metabolizer who was potentially vulnerable to paroxetine, a major inhibitor of CYP2D6. Heart failure is often accompanied by psychiatric disorders. A wide range of drugs commonly prescribed for these conditions, including beta-blockers, antiarrhythmics, and antidepressants, are metabolized by CYP2D6. Genetic screening for CYP2D6 in patients with these conditions may prevent life-threatening drug intoxication.
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PMID:Life-threatening serotonin syndrome in a patient with chronic heart failure and CYP2D6*1/*5. 1554 25

Chest pain presents a diagnostic challenge in outpatient family medicine. Noncardiac causes are common, but it is important not to overlook serious conditions such as an acute coronary syndrome, pulmonary embolism, or pneumonia. In addition to a thorough history and physical examination, most patients should have a chest radiograph and an electrocardiogram. Patients with chest pain that is predictably exertional, with electrocardiogram abnormalities, or with cardiac risk factors should be evaluated further with measurement of troponin levels and cardiac stress testing. Risk of pulmonary embolism can be determined with a simple prediction rule, and a D-dimer assay can help determine whether further evaluation with helical computed tomography or venous ultrasound is needed. Fever, egophony, and dullness to percussion suggest pneumonia, which can be confirmed with chest radiograph. Although some patients with chest pain have heart failure, this is unlikely in the absence of dyspnea; a brain natriuretic peptide level measurement can clarify the diagnosis. Pain reproducible by palpation is more likely to be musculoskeletal than ischemic. Chest pain also may be associated with panic disorder, for which patients can be screened with a two-item questionnaire. Clinical prediction rules can help clarify many of these diagnoses.
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PMID:Diagnosing the cause of chest pain. 1634 31

The catastrophic misinterpretation model [Behav. Res. Ther. 24 (1986) 461-470] proposes that panic attacks result from misinterpretation of interoceptive stimuli as precursors to physical or psychological emergency. Inconclusive evidence for the model may be partly explained by limitations of the questionnaires developed to measure catastrophic misinterpretation. For example, the Body Sensations Interpretation Questionnaire (BSIQ) is unable to clarify whether anxiety-related interpretations of ambiguous interoceptive stimuli represent catastrophic misinterpretations or responses masking feared outcomes (e.g., heart failure). Additionally, it lacks items relating to several DSM-IV criteria for panic, thereby limiting content validity. Reliability is also potentially compromised due to experimenter-coding of participant-generated responses. A modified form of the BSIQ was developed to address these limitations and evaluated with non-anxious controls (n=34) and people with panic disorder (n=38). The revised questionnaire demonstrated good to excellent internal consistency, inter-rater reliability, and construct validity and is a useful development of the BSIQ.
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PMID:Modification of the Body Sensations Interpretation Questionnaire (BSIQ-M): validity and reliability. 1646 7

According to the Khmer conception, a person suffering 'weak heart' (khsaoy beh daung) has episodes of palpitations on slight provocation (e.g. triggered by orthostasis, anger, a noise, worry, an odor or exercise) and runs the risk of dying of heart arrest during these periods of palpitations; too, the sufferer typically has other symptoms attributed to the purported cardiac dysfunction: fatigue, shortness of breath, and orthostatic dizziness. Many Khmer refugees suffer this cultural syndrome, an anxious-dysphoria ontology, most probably of French colonial provenance. The syndrome demonstrates considerable overlap with those Western illness categories that feature panic attacks, in particular post-traumatic stress disorder (PTSD) and panic disorder. In a psychiatric clinic survey, 60 percent (60/100) of those assessed believed themselves to currently suffer 'weak heart'; 90 percent (54/60) of those considering themselves to suffer from 'weak heart' thought that palpitations (e.g., those resulting from a loud noise or orthostasis) might result in death. The article illustrates the profoundly culturally constructed nature of 'cardiac sensations,' located in a specific historical trajectory and episteme; too, the article suggests that trauma may result more in panic disorder than 'PTSD' when autonomic arousal symptoms (in the present case, palpitations) are considered potentially life-threatening.
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PMID:The Khmer 'Weak Heart' Syndrome: Fear of Death from Palpitations. 2081 62

Approximately 1 percent of primary care office visits are for chest pain, and 1.5 percent of these patients will have unstable angina or acute myocardial infarction. The initial goal in patients presenting with chest pain is to determine if the patient needs to be referred for further testing to rule in or out acute coronary syndrome and myocardial infarction. The physician should consider patient characteristics and risk factors to help determine initial risk. Twelve-lead electrocardiography is typically the test of choice when looking for ST segment changes, new-onset left bundle branch block, presence of Q waves, and new-onset T wave inversions. For persons in whom the suspicion for ischemia is lower, other diagnoses to consider include chest wall pain/costochondritis (localized pain reproducible by palpation), gastroesophageal reflux disease (burning retrosternal pain, acid regurgitation, and a sour or bitter taste in the mouth), and panic disorder/anxiety state. Other less common but important diagnostic considerations include pneumonia (fever, egophony, and dullness to percussion), heart failure, pulmonary embolism (consider using the Wells criteria), acute pericarditis, and acute thoracic aortic dissection (acute chest or back pain with a pulse differential in the upper extremities). Persons with a higher likelihood of acute coronary syndrome should be referred to the emergency department or hospital.
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PMID:Outpatient diagnosis of acute chest pain in adults. 2341 61

Whether anxiety is a risk factor for a range of cardiovascular diseases is unclear. We aimed to determine the association between anxiety and a range of cardiovascular diseases. MEDLINE and EMBASE were searched for cohort studies that included participants with and without anxiety, including subjects with anxiety, worry, posttraumatic stress disorder, phobic anxiety, and panic disorder. We examined the association of anxiety with cardiovascular mortality, major cardiovascular events (defined as the composite of cardiovascular death, stroke, coronary heart disease, and heart failure), stroke, coronary heart disease, heart failure, and atrial fibrillation. We identified 46 cohort studies containing 2,017,276 participants and 222,253 subjects with anxiety. Anxiety was associated with a significantly elevated risk of cardiovascular mortality (relative risk [RR] 1.41, CI 1.13 to 1.76), coronary heart disease (RR 1.41, CI 1.23 to 1.61), stroke (RR 1.71, CI 1.18 to 2.50), and heart failure (RR 1.35, CI 1.11 to 1.64). Anxiety was not significantly associated with major cardiovascular events or atrial fibrillation although CIs were wide. Phobic anxiety was associated with a higher risk of coronary heart disease than other anxiety disorders, and posttraumatic stress disorder was associated with a higher risk of stroke. Results were broadly consistent in sensitivity analyses. Anxiety disorders are associated with an elevated risk of a range of different cardiovascular events, including stroke, coronary heart disease, heart failure, and cardiovascular death. Whether these associations are causal is unclear.
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PMID:Meta-Analysis of Anxiety as a Risk Factor for Cardiovascular Disease. 2783 34

It has long been known from microneurographic recordings in human subjects that the activity of postganglionic sympathetic axons occurs as spontaneous bursts, with muscle sympathetic nerve activity (MSNA) exhibiting strong cardiac rhythmicity via the baroreflex and skin sympathetic nerve activity showing much weaker cardiac modulation. Here we review the firing properties of single sympathetic neurons, obtained using highly selective microelectrodes. Individual vasoconstrictor neurons supplying muscle or skin, or sudomotor neurons supplying sweat glands, always discharge with a low firing probability (~30%) and at very low frequencies (~0.5 Hz). Moreover, they usually fire only once per cardiac interval but can fire greater than four times within a burst. Modeling has shown that this pattern can best be explained by individual neurons being driven by, on average, two preganglionic inputs. Unitary recordings of muscle vasoconstrictor neurons have been made in several pathophysiological states, including heart failure, hypertension, obstructive sleep apnea, bronchiectasis, chronic obstructive pulmonary disease, depression, and panic disorder. The augmented MSNA in each of these diseases features an increase in firing probability and discharge frequency of individual muscle vasoconstrictor neurons above that seen in healthy subjects, yet firing rates rarely exceed 1 Hz. However, unlike patients with heart failure, all patients with respiratory disease or panic disorder, and patients with hyperhidrosis, exhibited an increase in multiple within-burst firing, which emphasizes the different modes by which the sympathetic nervous system grades its output in pathophysiological states of high sympathetic nerve activity.
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PMID:Physiological and pathophysiological firing properties of single postganglionic sympathetic neurons in humans. 2914 91


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