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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the last few years, so many different substances produced by the endothelium have been discovered that this structure is considered today a paracrine organ. Among these substances, there are at least three with marked vascular effects: prostacyclin (PGI-2) and the endothelium-derived relaxing factor (EDRF) are vasodilators, platelet stabilizers and anti-atherogenic. On the other hand, endothelin-1 (ET-1) is a potent vasoconstrictor and probably pro-atherogenic. There are many agents that stimulate the liberation of these substances by the endothelium and most of them stimulate simultaneously the production of the three substances. Even though it is not possible yet to define the exact participation of the endothelium in the normal regulation of coronary blood flow it is highly probably that a disfunction of this structure secondary to hypercholesterolemia, hypertension, atheromatosis, diabetes and smoking may decrease the coronary reserve, induce coronary spasm and facilitates the development of atheroma.
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PMID:[Endothelium and coronary circulation]. 182 65

Most ischemic heart disease in associated with severe coronary atherosclerosis. A small subset of patients, however, had angina pectoris despite angiographically normal coronary arteries and absence of inducible coronary spasm. Coronary microcirculation (i.e. arteries too small to be visualized by current angiographic techniques) has been identified as the weak point of these patients. Small coronary vessel involvement may be due to organic conditions (such as diabetes, vasculitis, systemic collagen-vascular diseases, infectious processes) that act through coronary thrombosis or embolism and related alteration in coronary vasomotion; alternatively, the vascular abnormality appears to be entirely functional (no ultrastructural myocardial changes) such as the case of hypertension, hypertrophic cardiomyopathy and syndrome X. Whatever the cause(s) and mechanism(s) of the small coronary artery involvement, this leads to myocardial ischemia and to the related complications as in classic atherosclerotic heart disease. Syndrome X is characterized by effort-induced angina pectoris, ST-segment changes during exercise testing, negative ergonovine test and reduced coronary reserve. A pre-arteriolar hypersensitivity to vasoconstrictor influences (elicited by cold pressor test or ergonovine) and a reduced vasodilator capacity (unmasked by metabolic and pharmacological studies) have been proposed as potential pathogenetic substrate. This dynamic alteration in vasomotion would answer for both symptoms and signs of myocardial ischemia, that, however, appear to be contemporarily elicitable in a minority of patients. Treatment with beta-blockers and calcium-antagonists has been found to be effective. The long-term follow-up shows favorable outcome with a high survival rate and a low incidence of cardiovascular events.
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PMID:[Angina due to microvascular pathology]. 184 63

Calcium channel blockers are effective antihypertensive agents, both as initial monotherapy and in combination with other antihypertensive agents. These drugs are also effective in the treatment of chronic, stable angina, variant angina and supraventricular arrhythmias. Drugs in this class have different affinities for calcium channels in vascular smooth muscle, cardiac muscle, cardiac sinus and atrioventricular node. They are all useful in hypertension and angina, but only verapamil and diltiazem are also useful in the control of heart rate and supraventricular arrhythmias. Nimodipine may control vascular spasm following subarachnoid hemorrhage. Calcium channel blockers have also been used in the treatment of migraine headache and Raynaud's phenomenon.
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PMID:Comparative clinical pharmacology of calcium channel blockers. 199 Jul 41

Percutaneous rotational atherectomy (Rotablator), a high speed (greater than 100,000 RPM) rotational burr, was used successfully in 38 of 43 patients (88%) (mean age: 65 +/- 7 years) with 82 lesions (71 stenoses and 11 occlusions). The clinical indications were claudication (84%), nonhealing ulcer (7%), and renovascular hypertension (7%). Rotablation was successful in 78 of 82 lesions (95%): 68 of 71 (96%) stenoses (12 of 12 iliac, 11 of 11 femoral, 7 of 8 popliteal, 36 of 37 tibial, and 2 of 3 renal arteries; 60% of lesions were diffuse, i.e., greater than or equal to 4 cm in length), and 10 of 11 (91%) occlusions (5 of 6 femoral, 1 of 1 popliteal, 3 of 3 tibioperoneal, 1 of 1 brachial artery). The Rotablator significantly (p less than 0.001) reduced the arterial obstruction (stenoses: 85 +/- 11% to 12 +/- 12%); occlusions: 100% to 25 +/- 10%). The effective final burr size for arteries varied at 3.5-4.5 mm for renal, 3.0-3.5 mm for femoral, and 2.0-3.0 mm for brachial and tibial. Complications included gross hemoglobinuria without sequelae in 27 patients (63%), groin hematoma in 10 (23%), arterial spasm in 10 (23%), and arterial bypass in 2 (5%). The Rotablator was successfully used, without concomitant conventional balloon angioplasty, to open arterial lesions with excellent angiographic results in both diffuse and segmental peripheral vascular disease. There was gratifying patient clinical improvement.
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PMID:Acute angiographic and clinical outcome of high speed percutaneous rotational atherectomy (Rotablator). 201 77

Several new concepts are reviewed concerning structural and functional changes in atherosclerotic and hypertensive blood vessels. First, in regard to modulation of vascular changes, atherosclerosis appears to progress more slowly during hypotension than during normotension. This finding may have implications for the optimal level of blood pressure. Second, structural "remodeling" of the vessel wall occurs in both atherosclerosis and hypertension. Remodeling helps to preserve the arterial lumen despite intimal proliferation in atherosclerosis. In contrast, remodeling (which differs from vascular hypertrophy) reduces the vascular lumen in chronic hypertension. Third, functional changes impair active vasodilator responses in both atherosclerotic and hypertensive vessels, in part by endothelium-dependent mechanisms. Finally, we propose that leukocytes as well as platelets may be important cellular mediators of spasm in atherosclerotic arteries.
Hypertension 1991 Apr
PMID:Hemodynamic determinants of vascular changes in hypertension and atherosclerosis. 201 97

It was established that the ulceration zones showed hyperemia which increases the volume density of venous vessels, disturbs the permeability of their walls, causes trophic disorders with subsequent phlebosclerosis, limitation of capacitance, appearance of venous hypertension and further changes of the vessel wall structures and neighbouring tissues. Compensatory reaction of the arterial intraorganic bed (vascular spasm) deteriorates trophic disorders. Simultaneous increase of the volume density of arterial vessels in the "intact" zone favours reparative and compensatory capacities of the latter. Repeat ulcer formation and chronic course of the disease furthers development of hemo- and microcirculatory disorders, progressing of angio- and perivascular sclerosis, reorganization of the intramural gastric and duodenal vascular bed.
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PMID:[Changes in the intraorganic blood vessels of the stomach and duodenum in peptic ulcer]. 205 17

In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain, which, depending on a multitude of factors, can result in cerebral infarction. It is highly likely that the erythrocyte is the most important blood element in the pathophysiology of this process. The exact mechanism by which the blood vessel is forced into this destructive spasm remains to be elucidated. Significant steps have been taken to avoid the consequences of vasospasm by using hypertension and hypervolemia (or at the very least avoiding iatrogenic hypotension and hypovolemia). These measures have resulted in a reduced incidence of delayed ischemia. Because clot has been shown to cause vasospasm, it has seemed only logical that the early removal of clot would be efficacious in its prophylaxis. Experimental and clinical evidence to support this view has been gathered. Therapeutic measures based on it have been shown to be effective in the experimental situation but await controlled clinical evaluation. In the past decade, thanks to such trials, one of the calcium antagonist drugs has been shown to be effective in improving the outcome following subarachnoid hemorrhage, probably on the basis of reducing the frequency and extent of infarction by small vessel dilatation or neuronal protection. Although patients still die from this lethal complication of subarachnoid hemorrhage, it is difficult not to have some measure of optimism, based on the history just reviewed, that cerebral vasospasm will be a treatable disease within a few decades.
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PMID:The history of cerebral vasospasm. 213 40

Focal fibromuscular dysplasia of small coronary arteries is not so rare as it is unrecognized. Although sometimes occurring as an isolated abnormality, it more often accompanies a variety of other lesions including inflammation or infiltration. In this review based on personal study of over 1,000 human hearts, the 3 topics include a description of the morphologic characteristics of the lesion, a discussion of its functional consequences affecting coronary flow, and an iteration of theoretical explanations for its development. The typical lesion is focal in distribution, is comprised of both fibrous and smooth muscle elements, and the histologic organization is one of dysplastic array. Included among the subjects discussed in functional consequences are coronary spasm, coronary reserve, chest pain, electrical instability of the heart, and comments on the role of focal fibromuscular dysplasia of small coronary arteries in hypertension, myocardial hypertrophy and heart failure. Theories as to its development include primary faults of smooth muscle or collagen, and focal abnormalities of clotting or neurovascular relation, but it is likely that the cause is multifactorial.
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PMID:Morphologic characteristics and functional significance of focal fibromuscular dysplasia of small coronary arteries. 218 50

After smoking "crack" cocaine and consuming large quantities of ethanol, a 36-year-old man developed multiple, bilateral, deep, and superficial cerebral hematomas. He was hypertensive for several days, but angiography revealed no evidence of vascular malformation or vasculitis. The multifocality of the hematomas and lack of underlying disease suggest that the hemorrhages resulted from cocaine-induced acute hypertension or arterial spasm, possibly potentiated by heavy ethanol consumption.
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PMID:Multiple intracerebral hemorrhages after smoking "crack" cocaine. 219 Mar 62

We conducted a study on the clinical and angiographic characteristics of 140 patients with unstable angina. Average age of 57, male/female ratio 4 to 1. The most frequent risk factors: tobacco smoking (73%) and arterial hypertension (42%). They had old infarct (57%), and unstable angina at rest (37%). We did early submaximal stress test to 31% of them; in 38.6% test was stopped due to angina, 25% for fatigue. 91% had ischemic changes, there weren't any severe complications. Regarding significant coronary obstruction: 20% had one vessel, 26% two, 50% three and left trunk 4%. Normal ventriculogram 43%. Eight patients died; the causes were: disease of the trunk (37.5%) and "active" angina (87.5%), 25% during catheterization . All survivors responded to medical treatment. 54 patients were not candidates for surgical treatment, among them 70.3% were released in class I (NYHA). At follow up 90% were in class I-II, 12% had unstable angina recurrence, 3% had acute infarct. In the pathogenesis of unstable angina intervene fixed atherosclerosis, obstructive lesions, repetitive spasms and non-occlusive thrombosis, this physiopathologic behavior is responsible for the stages of ischemic activity. Treatment should be directed to maintain the balance between the distribution and the demand of O2, and also treating spasm and thrombosis.
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PMID:[Unstable angina: clinical and angiographic characteristics of 140 cases]. 224 1


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