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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 46-year-old man was hospitalized with paroxysmal headache and chest discomfort. His blood pressure varied, occasionally being up to 300/160 mmHg. Cardiac examination revealed a decrescendo type of diastolic murmur (aortic regurgitation) and S4 gallop. Both blood and urine catecholamine levels were extremely high. Electrocardiogram and echocardiogram showed severe left ventricular hypertrophy pattern presenting hypertrophic cardiomyopathic changes. The phonocardiogram showed marked Hegglin syndrome (QT; 450 msec and QII; 310 msec). Right adrenal tumor, pheochromocytoma was found on the abdominal CT scanning and 131I-metaiodobenzylguanidine (MIBG). In the post-operative period, Hegglin syndrome was completely abolished (QT; 360 msec and QII; 345 msec,), and also electrocardiographic left ventricular hypertrophy pattern improved immediately after surgical removal of the pheochromocytoma.
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PMID:[A marked Hegglin syndrome in pheochromocytoma]. 273 13

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

We report the findings in a patient in whom torsade de pointes atypical ventricular tachycardia occurred as a complication of subarachnoid hemorrhage. The patient was a 54-year-old female and she was admitted to our hospital to treat gastric ulcer on October 8, 1985. The electrocardiogram on admission showed mild left ventricular hypertrophy. She complained of severe headache and nausea in hospital on November 10 and she was transferred to our department. Her consciousness was clear. Computed tomography revealed a subarachnoid hemorrhage and left carotid angiogram showed a left middle cerebral artery aneurysm. Laboratory findings of blood and a chest roentgenogram were normal, but the electrocardiogram revealed a prominent prolongation of the QT interval and generalized giant negative T waves. The aneurysm was clipped on November 11, but a torsade de pointes atypical ventricular tachycardia occurred after clipping of the aneurysm during the surgery. Several anti-arrhythmic agents were not effective but phenytoin suppressed the arrhythmia. Postoperative course was almost uneventful. Since she had mild right hemiparesis, she continued the rehabilitation in our department. Five months later her electrocardiographic findings became normal. Prolongation of the QT interval and the giant negative T wave are typical electrocardiographic abnormalities in patients of subarachnoid hemorrhage, causing a predisposition to torsade de pointes ventricular tachycardia. The arrhythmia should be kept in mind as a complication in a viewpoint of the management of subarachnoid hemorrhage in the acute stage.
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PMID:[An electrocardiographic abnormality called torsade de pointes in a patient of subarachnoid hemorrhage]. 339 96

A hypertensive urgency should be distinguished from a hypertensive emergency. Although the distinction may not always be obvious, certain guidelines may help the clinician determine which therapeutic approaches are most appropriate for each patient. Hypertensive emergencies include those conditions in which new or progressive severe end-organ damage is present and a delay in appropriate therapy might result in permanent damage, progression of complications, and a poor prognosis. Hypertensive urgencies include those conditions with minimal to no obvious end-organ damage in which blood pressure should be lowered expeditiously. The risk of immediate complications or organ damage is less likely to occur, and thus the immediate prognosis is better, although the ultimate prognosis, if untreated, is poor. There is a marked individual, racial, sexual, and age difference in the ability to tolerate high intraarterial pressure, as evidenced by patients' symptoms and signs of end-organ damage. Patients may have no symptoms of elevated blood pressure until significant intraarterial levels are reached. If symptoms are present, they may include headache, dizziness, blurred vision, shortness of breath (especially with exertion), chest pain, rapid pulse, palpitations, malaise and fatigue, nocturia, or pedal edema. Signs of hypertensive disease vary and depend not only on the level of blood pressure but also include funduscopic changes with arteriolar narrowing, atrioventricular nicking, hemorrhages, exudates or papilledema, central nervous system changes and neurologic abnormalities, cardiac changes with gallop rhythm, cardiomegaly, tachycardia, ectopic ventricular beats, left ventricular hypertrophy or signs of congestive heart failure, pulmonary edema, and signs of renal insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive emergencies and urgencies: pathophysiology and clinical aspects. 394 53

This report describes a young woman with unexplained chronic hypoventilation that was greatly exacerbated during sleep. Treatment with nocturnal O2 during a 2-yr period was associated with stable cardiovascular function but severe morning headaches and lethargy, presumably related to nightly bouts of hypercapnia and acidosis during sleep. A subsequent 2-yr period in which ventilation was assisted during sleep by means of a rocking bed, but supplementary O2 was not used, was associated with disappearance of the headaches and improved psychosocial function, but with the insidious development of signs of pulmonary hypertension and right ventricular hypertrophy. This patient's clinical course demonstrates the separate adverse effects of intermittent hypoxemia and hypercapnia and emphasizes the importance of preventing both hypoxemia and hypercapnia during sleep.
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PMID:Idiopathic hypoventilation syndrome: importance of preventing nocturnal hypoxemia and hypercapnia. 735 98

Although an association between oral contraceptives (OCs) and arterial hypertension has been well-documented, most studies have found only mild or moderate hypertension with reversal to normal levels 3 months after OC discontinuation. This paper presents two cases in which young women developed severe left ventricular hypertrophy and renal failure due to OC-induced malignization of hypertension. The first patient, a 23-year-old, was admitted to the hospital with a 3-day history of headache, mental confusion, and aggressiveness. 6 months before presentation, severe arterial hypertension had been diagnosed. At that time, she was advised to discontinue OCs (30 mcg of ethinyl estradiol and 150 mcg of levonorgestrel), which she had been taking for a year; she did not comply with this directive. The second patient, 21 years old, was admitted with accelerating hypertension. She had initiated OC use (30 mg of ethinyl estradiol and 150 mcg of levonorgestrel) 6 months earlier. 3 months after starting OC use, she developed headache and fatigue. Both women had a hemorrhagic cerebral accident as a complication of malignant hypertension. All neurologic, renal, and cardiovascular complications were reversible after OC discontinuation. OC-related malignant hypertension can be averted through effective control of blood pressure in OC users.
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PMID:Cardiac and neurologic complications in malignant hypertension due to oral contraceptive use. 786 96

Obstructive sleep apnea (OSA) syndrome occurs in 4% to 9% of middle-aged men and in 1% to 2% of middle-aged women. The incidence of OSA among morbidly obese patients is 12- to 30-fold higher. The pathophysiology of OSA is complex and incompletely understood. The important clinical symptoms of OSA include snoring, daytime sleepiness, restless sleep, morning fatigue, and headaches. The diagnosis is made by polysomnography. The possible sequelae of OSA are hypertension, left and right ventricular hypertrophy, sudden cardiovascular death, and increased risk for brain infarction. Nasal continuous positive airway pressure (nCPAP) appears to be the recommended treatment for OSA. Morbidly obese patients may also benefit from weight reduction gastric surgery.
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PMID:Obstructive sleep apnea in the obese. 971 28

The TEAM trial investigated the effectiveness and tolerance of a fixed combination of the ACE inhibitor and calcium channel blocker (2 mg trandolapril and 180 mg verapamil retard) (preparation Tarka) in an open multicentre prospective study of treatment of moderately severe hypertension (diastolic pressure at the end of the two-week wash-out period 100-115 mm Hg). The trial comprised 163 patients who were treated first for four weeks by a monotherapy with 2 mg trandolapril. After these four weeks patients who attained normal blood pressure proceeded with trandolapril treatment. Hypertensive patients who did not attain normal diastolic pressure levels were treated for another four weeks by a fixed combination of trandolapril and verapamil SR. After four weeks of treatment with trandolapril 62 patients of 163 (37%) had a diastolic blood pressure of less than 90 mm Hg. The fixed combination of trandolapril and verapamil SR reduced the diastolic blood pressure to less than 90 mm Hg in 71.6% of the patients resistant to treatment with 2 mg trandolapril and in another 15.6% of patients it reduced the diastolic blood pressure by 10 mm Hg or more. After two months of treatment 60 patients had a normal blood pressure due to trandolapril (37%) and another 73 patients (45%) treated by a combination of trandolapril and verapamil SR, i.e. a total of 133 patients (82%) who originally suffered from moderately severe hypertension, attained a normal diastolic blood pressure. The mean decrease of diastolic pressure after two months of treatment was 19.5 mm Hg in "non-respondents" to trandolapril monotherapy and 23.6 mm Hg in "respondents". The mean decrease of systolic pressure in "non-respondents" and "respondents" after trandolapril treatment was 19.5 mm Hg and 35.0 mm Hg resp. The fixed combination of trandolapril and verapamil was not only effective but was associated with a minimum of undesirable effects. The incidence of headaches declined significantly. The combination of the above preparations is useful also because both preparations have a cardio- and nephroprotective effect and do not affect the lipid and carbohydrate metabolism. Treatment with a fixed combination of trandolapril and verapamil SR is indicated in moderately severe hypertension not responding to monotherapy, in particular when associated with diabetes, hyperlipoproteinaemia, ischaemic heart disease or left ventricular hypertrophy.
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PMID:[The TEAM study--a study of the effectiveness and tolerance of treatment of essential hypertension with a fixed combination of trandolapril and verapamil]. 982 54

We present a single-blinded, placebo-controlled trial of the effects on blood pressure and left ventricular mass and of the safety of a combined antihypertensive treatment with delapril, a new nonsulfhydryl angiotensin-converting enzyme inhibitor, and indapamide, a sulfonamide diuretic. We studied 28 elderly patients aged 65-85 years (mean age, 69 +/- 1) with sitting systolic/diastolic blood pressure of 160-200/95-115 mm Hg (at the end of the placebo period). After a 2-week placebo run-in, patients took 30 mg delapril in combination with 1.25 mg indapamide once daily for 24 weeks. Twenty-four-hour ambulatory blood pressure was monitored and M- and B-mode echocardiography were performed before and after 24 weeks of treatment. Blood pressure decreased from 156 +/- 1.5/101 +/- 1 mm Hg before treatment to 133 +/- 1/73 +/- 1 mm Hg after treatment. The total blood pressure burden also decreased; the percentage of measurements with a systolic blood pressure > or = 140 mm Hg and a diastolic blood pressure > or = 90 mm Hg decreased from 48.7% +/- 5%/31.5% +/- 4.3% to 23.5% +/- 4%/20.5% +/- 2.9% (p < 0.0005 and p < 0.05). The area under the curve of the 24-hour blood pressure decreased from 250 +/- 41/103 +/- 21 mm Hg to 97 +/- 21/37 +/- 8.5 mm Hg (p < 0.001 and p < 0.005). The left ventricular mass index (LVMI) in the 15 patients with pretreatment left ventricular hypertrophy was reduced after therapy from 167.5 +/- 8.5 g/m 2 to 152.2 +/- 7.6 g/m 2 (p < 0.05). A positive correlation was observed between percent changes of the area under the curve of the 24-hour diastolic blood pressure and percent changes of LVMI (r = 0.6; p < 0. 05) in the 15 patients with left ventricular hypertrophy. Only 2 patients reported side effects: 1 developed skin rash and 1 developed headache. The safety of the treatment was confirmed by laboratory tests. In elderly hypertensive patients, the combination of delapril and indapamide at low doses reduced blood pressure and had favorable effects on LVMI with few side effects.
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PMID:Effects of delapril in combination with indapamide on blood pressure and left ventricular mass in elderly hypertensive patients. 1009 33

Angiotensin II receptor blockers (ARBs) represent a new class of effective and well tolerated orally active antihypertensive agents. Recent clinical trials have shown the added benefits of ARBs in hypertensive patients (reduction in left ventricular hypertrophy, improvement in diastolic function, decrease in ventricular arrhythmias, reduction in microalbuminuria, and improvement in renal function), and cardioprotective effect in patients with heart failure. Several large long-term studies are in progress to assess the beneficial effects of ARBs on cardiac hypertrophy, renal function, and cardiovascular and cerebrovascular morbidity and mortality in hypertensive patients with or without diabetes mellitus, and the value of these drugs in patients with heart disease and diabetic nephropathy. The ARBs specifically block the interaction of angiotensin II at the AT1 receptor, thereby relaxing smooth muscle, increasing salt and water excretion, reducing plasma volume, and decreasing cellular hypertrophy. These agents exert their blood pressure-lowering effect mainly by reducing peripheral vascular resistance usually without a rise in heart rate. Most of the commercially available ARBs control blood pressure for 24 h after once daily dosing. Sustained efficacy of blood pressure control, without any evidence of tachyphylaxis, has been demonstrated after long-term administration (3 years) of some of the ARBs. The efficacy of ARBs is similar to that of thiazide diuretics, beta-blockers, angiotensin-converting enzyme inhibitors or calcium channel blockers in patients with similar degree of hypertension. Higher daily doses, dietary salt restriction, and concomitant diuretic or ACE inhibitor administration amplify the antihypertensive effect of ARBs. The ARBs have a low incidence of adverse effects (headache, upper respiratory infection, back pain, muscle cramps, fatigue and dizziness), even in the elderly patients. After the approval of losartan, five other ARBs (candesartan cilexetil, eprosartan, irbesartan, telmisartan, and valsartan) and three combinations with hydrochlorothiazide (irbesartan, losartan and valsartan) have been approved as antihypertensive agents, and some 28 compounds are in various stages of development. The ARBs are non-peptide compounds with varied structures; some (candesartan, losartan, irbesartan, and valsartan) have a common tetrazolo-biphenyl structure. Except for irbesartan, all active ARBs have a carboxylic acid group. Candesartan cilexetil is a prodrug, while losartan has a metabolite (EXP3174) which is more active than the parent drug. No other metabolites of ARBs contribute significantly to the antihypertensive effect. The variation in the molecular structure of the ARBs results in differences in the binding affinity to the receptor and pharmacokinetic profiles. The differences observed in lipid solubility, absorption/distribution, plasma protein binding, bioavailability, biotransformation, plasma half-life, and systemic elimination influence the time of onset, duration of action, and efficacy of the ARBs. On the basis of the daily mg dose, the antihypertensive potency of the ARBs follows the sequence: candesartan cilexetil > telmisartan approximately = losartan > irbesartan approximately = valsartan > eprosartan. After oral administration, the ARBs are rapidly absorbed (time for peak plasma levels = 0.5-4 h) but they have a wide range of bioavailability (from a low of 13% for eprosartan to a high of 60-80% for irbesartan); food does not influence the bioavailability, except for valsartan (a reduction of 40-50%) and eprosartan (increase). A limited dose-peak plasma levels/areas under the plasma level-time curve proportionality is observed for some of the ARBs. Most of these drugs have high plasma protein binding (95-100%); irbesartan has the lowest binding among the group (90%). The steady-state volumes of distribution vary from a low of 9 L (candesartan) to a high of 500 L (telmisartan). (ABSTRACT TRUNCATE
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PMID:Clinical pharmacokinetics of angiotensin II (AT1) receptor blockers in hypertension. 1085 85


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