Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postural tachycardia syndrome (POTS) is a disabling condition that commonly affects otherwise normal young females. Because these patients can present with a flushing disorder, we hypothesized that mast cell activation (MCA) can contribute to its pathogenesis. Here we describe POTS patients with MCA (MCA+POTS), diagnosed by episodes of flushing and abnormal increases in urine methylhistamine, and compared them to POTS patients with episodic flushing but normal urine methylhistamine and to normal healthy age-matched female controls. MCA+POTS patients were characterized by episodes of flushing, shortness of breath, headache, lightheadedness, excessive diuresis, and gastrointestinal symptoms such as diarrhea, nausea, and vomiting. Triggering events include long-term standing, exercise, premenstrual cycle, meals, and sexual intercourse. In addition, patients were disabled by orthostatic intolerance and a characteristic hyperadrenergic response to posture, with orthostatic tachycardia (from 79+/-4 to 114+/-6 bpm), increased systolic blood pressure on standing (from 117+/-5 to 126+/-7 mm Hg versus no change in POTS controls), increased systolic blood pressure at the end of phase II of the Valsalva maneuver (157+/-12 versus 117+/-9 in normal controls and 119+/-7 mm Hg in POTS; P=0.048), and an exaggerated phase IV blood pressure overshoot (50+/-10 versus 17+/-3 mm Hg in normal controls; P<0.05). In conclusion, MCA should be considered in patients with POTS presenting with flushing. These patients often present with a typical hyperadrenergic response, but beta-blockers should be used with great caution, if at all, and treatment directed against mast cell mediators may be required.
Hypertension 2005 Mar
PMID:Hyperadrenergic postural tachycardia syndrome in mast cell activation disorders. 1571 Jul 81

In elderly patients, an inadequately treated high blood pressure often leads to hypertrophied cardiomyocytes with various defects in gene expression. Due to a decreased expression of the transcription factor PPARalpha, fatty acid oxidation is reduced. If it can be compensated by an increased glucose oxidation, it has been considered as a favorable process. Nonetheless, reduced PPARalpha influences ensue involving e. g. anti-inflammatory mechanisms. The question arises thus whether drugs can normalize reduced PPARalpha effects without increasing fatty acid oxidation. As lead compound of these "fatty acid oxidation inhibitors with PPARalpha activation", the carnitine palmitoyltransferase-1 inhibitor etomoxir was characterized. An increased expression and activity of the Ca (2+) pump of sarcoplasmic reticulum, a faster relaxation and a slowed progression of heart failure was observed in animal experiments. It should, therefore, be examined whether the impaired function of pressure overloaded hypertrophied cardiomyocytes of particularly elderly patients should be a therapeutic target before progression of heart failure, neuroendocrine activation and symptoms such as shortness of breath occur.
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PMID:[Metabolism and the hypertrophied heart of the elderly]. 1577 59

Zygomycosis is an uncommon but frequently fatal infection and occurs mostly in immunosuppressed hosts, whereas approximately 50% of zygomycosis occurs in diabetic patients. The current patient initially presented with persistent pulmonary edema secondary to renal failure. This was the last of four admissions within 1 year for this 68-year-old woman, for whom the chief complaints were shortness of breath and chest pain. Her past medical history included insulin-requiring type 2 diabetes and hypertension for 10 years, and chronic heart and renal failure. She was previously admitted to the hospital for what appeared to be pulmonary edema secondary to renal failure. In the last admission the patient developed pulmonary hemorrhage and metabolic acidosis. Transbronchial biopsy was performed, showing irregular fungal hyphae in the blood vessels, morphologically consistent with zygomycosis. Central nervous system computed tomography also revealed a large infarct in the cerebral hemisphere. The patient died on the seventh hospital day. At autopsy three organs were extensively involved by zygomycosis: (i) lungs were diffusely hemorrhagic with acute infarcts; (ii) pericardium had fibrotic inflammation; and (iii) the left cerebral hemisphere, cerebellum and pons had large hemorrhagic infarct by zygomycosis infection. Corticosteroid medication and hemodialysis triggered increasing hyperglycemia, metabolic acidosis and iron overload, which contributed to zygomycosis infection that subsequently spread to the heart and brain as a rare consequence.
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PMID:Zygomycosis involving lungs, heart and brain, superimposed on pulmonary edema. 1582 46

An 81-year-old woman presented with shortness of breath and fever of 3 days duration. An enhanced CT of the chest revealed a patent ductus arteriosus (PDA) communicating with the true lumen of an aortic arch dissection. Neither the aortic dissection nor the PDA was suspected. The patient had no history of a connective tissue abnormality or other condition which would predispose to dissection other than systemic hypertension. It is likely that propagation of the aortic dissection partially re-opened the ductus arteriosus.
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PMID:Aortic dissection with extension to a patent ductus arteriosus. 1604 30

56 year-old male presented to the University of Mississippi Medical Center emergency department (ED) with complaints of progressive shortness of breath, productive cough, fever, and malaise. His past medical history was significant for hypertension as well as a 60 pack-year history of smoking. Upon arrival to the ED he had a temperature of 103.6 degrees F, blood pressure of 80/40 mm Hg, a pulse of 110 beats per minute, respirations of 28 per minute, and an oxygen saturation of 50% on room air. He appeared to be in significant respiratory distress. Lung examination revealed diffuse bilateral rhonchi and wheezes in all lung fields. He was emergently intubated. Chest radiograph demonstrated a miliary pattern scattered throughout all lung fields in addition to parenchymal opacities. A complete blood count revealed a white blood cell count of 33,500 10(3)/microL, hematocrit of 37%, and platelets of 906,000 10(3)/uL. Blood urea nitrogen and creatinine were 27 mg/dL and 1.0 mg/dL, respectively. Initial ABG on 100% oxygen showed pH 7.15, pCO2 82 mm Hg, and pO2 62 mm Hg. Troponin I was negative. An electrocardiogram demonstrated sinus tachycardia. Blood and urine cultures were obtained.
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PMID:Mystery in the basement. 1611 97

Noncardiogenic pulmonary edema is a rare but potentially life-threatening complication of hydrochlorothiazide therapy. We describe three patients who developed this serious adverse reaction. A 64-year-old woman developed dypsnea and hypotension within 60 minutes of taking a single dose of hydrochlorothiazide 25 mg. She was admitted to the critical care unit with acute respiratory failure and subsequent multiple-organ dysfunction. The second patient was a 56-year-old woman who experienced sudden onset of shortness of breath that developed 10 minutes after taking a single dose of hydrochlorothiazide 25 mg. The third was a 59-year-old woman who developed sudden onset of shortness of breath, nausea, vomiting, and diarrhea after her first dose of hydrochlorothiazide-triamterene. All three women had a history of a similar, albeit minor, reaction to a thiazide diuretic. Review of the literature identified 36 additional cases of noncardiogenic pulmonary edema after thiazide use. The patients developed symptoms 10-150 minutes after ingestion of hydrochlorothiazide or another thiazide. Symptoms can occur on first exposure to the drug or in patients taking the drug intermittently. Of interest, 90% of documented cases occurred in women. With the increasing use of thiazide diuretics in the treatment of hypertension, clinicians need to be aware of the possible association of these drugs with the development of noncardiogenic pulmonary edema.
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PMID:Hydrochlorothiazide-induced noncardiogenic pulmonary edema: an underrecognized yet serious adverse drug reaction. 1616 99

Erythropoietin is a hypoxia-induced hormone that is a major regulator of normal erythropoiesis. Over the last decade, the production of recombinant human erythropoietin has revolutionized the treatment of anemia associated with chronic renal failure, and has led to a greater understanding of anemia pathophysiology and to the elucidation of the interactions of erythropoietin, iron, and erythropoiesis. Anemia has been shown to be independently associated with increased mortality and disease progression. Potential survival benefits associated with correction of anemia have expanded considerably the indications of erythropoietin use in various patient populations and are leading to consideration of earlier, more aggressive treatment of mild to moderate anemia. The results of such treatment are promising in a variety of new clinical settings, including anemia associated with congestive heart failure. Furthermore, the erythropoietin receptor is widely distributed in the cardiovascular system, including endothelial cells, smooth muscle cells and cardiomyocytes and preclinical studies have established erythropoietin to be a pleiotropic cytokine with anti-apoptotic activity and tissue-protective actions in the cardiovascular system, beyond correction of hemoglobin levels. Despite some potential adverse effects, such as hypertension, and the occurrence of erythropoietin resistance, early studies in heart failure patients with anemia suggest that erythropoietin therapy is safe and effective in reducing left ventricular hypertrophy, enhancing exercise performance and increasing ejection fraction. Anemia is found in about one-third of all cases of congestive heart failure (CHF). The most likely common cause is chronic renal insufficiency, which is present in about half of all CHF cases. However, anemia can occur in CHF without renal insufficiency and is likely to be due to excessive cytokine production. The anemia itself can worsen cardiac function, both because it causes cardiac stress through tachycardia and increased stroke volume, and because it can cause a reduced renal blood flow and fluid retention, adding further stress to the heart. Long-standing anemia of any cause can cause left ventricular hypertrophy, which can lead to cardiac cell death through apoptosis and worsen CHF. Therefore, a vicious circle, cardio-renal anemia syndrome, is set up wherein CHF causes anemia, and the anemia causes more CHF and both damage the kidneys worsening the anemia and the CHF further and increasing mortality. There is now evidence that early correction of the CHF anemia with subcutaneous erythropoietin and intravenous iron improves shortness of breath and fatigue, cardiac function, renal function and exercise capacity, reducing the need for hospitalization and improving quality of life. In the present review we discuss the data on current clinical use of erythropoietin in cardiovascular disease, with the main focus on the treatment of congestive heart failure, and summarize the advances and progress made in the understanding of the hematopoietic and pleiotropic effects of erythropoietin in the cardiovascular system.
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PMID:Erythropoietin in heart failure and other cardiovascular diseases: hematopoietic and pleiotropic effects. 1624 29

Prior to anesthesia a 65-year-old patient received 8 mg dexamethasone to prevent postoperative nausea and vomiting (PONV). Instantly she reported tingling and burning followed by intense pain in the genital region spreading to the whole body. Shortly later she complained about shortness of breath and pre-cordial pain. Acute hypertension could only be lowered by NTG, beta-blockade and induction of anesthesia. The ECG showed ST-segment depressions and troponin-T was elevated (0.3 ng/ml). Coronary angiography revealed no significant stenosis and an abdominal CT scan showed no evidence of a pheochromocytoma. Urine metabolites of catecholamines were negative. Thus, the most likely diagnosis was stimulation of endogenous catecholamines by painful stress after dexamethasone injection with the consequence of myocardial ischemia. As a result we now routinely inject dexamethasone after anesthesia induction as prophylaxis for PONV.
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PMID:[Acute hypertension following dexamethasone. A critical incident during anesthesia]. 1662 58

Immigrants from the former Soviet Union have a higher prevalence of cardiac risk factors and more problems obtaining health care in the United States than American-born Caucasians. This study compared differences between patients of these two populations admitted for diagnosis of chest pain or shortness of breath. Immigrants from the former Soviet Union (who had been in the U.S. for an average of 20 years) had more cardiac risk factors than American-born Caucasians including more hypertension (81% vs. 50%, p=.002), positive family history (53% vs. 30%, p=.030), more previous heart attacks (45% vs. 20%, p=.012), more prior cardiac catheterizations (51% vs. 18%, p<.001) and coronary revascularization procedures (51% vs. 27%, p=.022), and higher systolic blood pressure (138+/-13 vs. 129+/-23 mmHg, p=.019) upon presentation to the hospital. Fifty-five percent of immigrant patients used foreign medications. Thus, there are major differences between immigrants from the former Soviet Union who are admitted to the cardiac units of an urban New York hospital and American-born Caucasians. Knowledge of these differences is important for caregivers.
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PMID:Cardiac risk factors, medicine usage, and hospital course in immigrants from the former Soviet Union. 1670 16

In our study we have examined 198 patients admitted to hospital for shortness of breath at rest due to left ventricle failure. We have divided the patients into two groups according to the presence of diabetes mellitus. We have excluded the patients with noncardiac cause of pulmonary congestion, with valvular or congenital heart disease and with acute coronary syndromes. We have evaluated the presence of hypertension, value of blood sugar on admission, systolic and diastolic blood pressure, heart rate and medication given for heart insufficiency. We have also compared two dimensional transthoracal echocardiogaphic examination in diabetics to nondiabetics. Finally we compared hospital mortality in both groups. Diabetes mellitus (all the patients were type 2 diabetics) was present in 94 patients (47,5 %), in the group of diabetics there were 50 women, in nondiabetics 52 women (n.s.). The average age of diabetics was 75,5 +/- 8 years and 76,6 +/- 10,1 years in nondiabetics (n.s.). History of hypertension had 45 nondiabetics (43 %) and 69 diabetics (73,5 %), p < 0.05. Systolic blood pressure was significantly higher in diabetics 151 +/- 20,8 mm Hg to 140,5 +/- 18,4 mm Hg in nondiabetics, p < 0.05. The values of diastolic pressure and heart rate were comparable in both groups. We have not noticed any significant difference in the application of ACE inhibitors, beta blockers and diuretics for heart failure in both groups. Echocardiographic examination revealed the significantly higher ejection fraction of left ventricle in diabetics as well as the thicker septum and posterior wall of left ventricle. These findings support the role of the diastolic dysfunction in pathogenesis of left ventricle failure. In hospital mortality rate was 8,5 % in diabetics and 7,6 % in nondiabetics (n.s.). Our results confirmed that in pathogenesis of left ventricle failure hypertension and elevated systolic blood pressure play the important part. Apart from the complex secondary prevention of ischemic heart disease the correct treatment of hypertension represents the very important part of the prevention of left ventricle failure. The role of the proper compensation of diabetes mellitus in the prevention of left ventricle failure is also discussed.
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PMID:[The comparison of clinical and echocardiographic changes in diabetics 2nd type and nondiabetics in patients with shortness of breath due to left ventricular failure]. 1673 36


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