Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
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The plasma activities of LDH and ASAT isoenzymes as well as of DP IV were studied in patients with essential hypertension and related to blood pressure, haemodynamic indicators of latent heart failure and to ischaemic heart risk indicators. Patients with elevated systolic or diastolic blood pressure showed significantly increased activities of ASAT m. In hypertensives with elevated pulmonary artery pressure markedly increased activities of ASAT, ASAT m, LDH M and DP IV could be observed. Distinctly increased activities of ASAT, ASAT m, LDH M and DP IV were also found in patients with elevated plasma cholesterol. The results obtained suggest that changes of LDH and ASAT isoenzymes as well as of DP IV indirectly reflecting alterations in organ metabolism might provide useful additional information with respect to uncovering hypertension-linked complications.
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PMID:Isoenzyme (lactate dehydrogenase, aspartate aminotransferase) and dipeptidyl peptidase IV activity changes in blood plasma likely indicative of organ involvement due to arterial hypertension. 168 Jun 2

Radiotracer methods were used to measure the rates of regional release of adrenaline and noradrenaline into plasma in man. This was done as a partial test of a theory of essential hypertension pathogenesis which envisages an important cotransmitter function for neuronally released adrenaline. In healthy resting men no release of adrenaline could be detected from the heart, lungs or liver. Adrenaline was released into the right renal vein but an adrenal medullary source is suspected. With the relatively limited activation of the cardiac sympathetic outflow which accompanied mental challenge and isometric exercise, cardiac adrenaline release remained undetectable. During supine bicycle exercise, which increased cardiac noradrenaline release 10-30 fold, to a mean value of 197 ng/min, cardiac adrenaline release averaged 2.36 ng/min. In two clinical conditions associated with persistently elevated plasma adrenaline concentrations, cardiac failure and adrenaline-secreting phaeochromocytoma, regional release of adrenaline was clearly evident. Thus, in normal man during exercise, and in patients with cardiac failure at rest, adrenaline is released from non-adrenal sources, and probably from sympathetic nerves. Whether neuronal adrenaline release of the degree found would be sufficient to facilitate noradrenaline release, augment sympathetically-mediated cardiovascular responses and contribute to the development of arterial hypertension remains to be tested.
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PMID:Is adrenaline released by sympathetic nerves in man? 182 56

A study was made of the concentration of endothelin (ET) in the plasma of patients suffering from arterial hypertension (AH), heart failure (HF) and in that of healthy volunteers. The concentration of ET in the normal subjects was within 4.0-8.6 pg/ml, in the patients with AH, it varied from 5.7 to 64.5 pg/ml, and in the patients suffering from HF, from 8.8 to 94.0 pg/ml. A subgroup of patients with essential hypertension, stage II B, showed a tendency towards a rise of the ET concentration in response to orthostatic load that was associated with an increase of the concentration of angiotensin-2.
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PMID:[Endothelin in arterial hypertension]. 182 61

The pathogenesis of essential hypertension may possibly involve a deficiency in, or a decreased response to, endogenous vasodilator and natriuretic factor(s). Searching for hereditary or familial defects, it is plausible to evaluate blood pressure (BP) regulating factors in (yet) normotensive offspring of hypertensive parents (OHyp), some of whom are in fact in a stage of prehypertension. Studies by our group demonstrated that compared with healthy offspring of normotensive parents, OHyp have plasma atrial natriuretic (ANF) factor levels that are unaltered on a low salt intake but often fail to increase normally in response to a high salt intake. Plasma levels of cyclic GMP, the presumed second messenger of ANF, also may tend to be decreased in certain OHyp. On the other hand, renal excretory responses of cyclic GMP and electrolytes to ANF infused in "physiological" dose were unchanged in some OHyp tested so far. In borderline to moderate, uncomplicated essential hypertension, plasma ANF levels are often "normal." This may be inappropriately low relative to the existing BP, although the relationship of circulating ANF to atrial pressures in essential hypertension remains to be clarified. A conversion to higher plasma ANF values may occur with cardiac complications such as left ventricular hypertrophy, enlargement, dysfunction, or overt heart failure. Acute or short-term elevation of circulating ANF within the physiological and pathophysiological range by ANF infusion produces an exaggerated natriuresis and lowers BP in essential hypertensive patients. We postulate a syndrome of ANF deficiency, characterized by an impaired response of circulating ANF to high salt intake and by low cyclic GMP levels in certain yet normotensive offspring of essential hypertensive parents and by inappropriately "normal" plasma ANF in some patients with uncomplicated essential hypertension. At the stage of prehypertension, a disturbance in the ANF - cyclic GMP pathway may be expressed primarily at the circulatory rather than at the renal level. Hypertension-prone humans also tend to have an exaggerated vascular reactivity to norepinephrine. Whether the two disturbances may be interrelated is presently unknown. Both defects may potentially predispose to the development of essential hypertension. Relative ANF deficiency, an enhanced natriuretic response to ANF, and a sustained antihypertensive effect of infused ANF may represent a rational basis for treatment of essential hypertension with agents that activate the ANF system.
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PMID:Developing essential hypertension: a syndrome involving ANF deficiency? 183 26

In essential hypertension, ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal, even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). One of the profound mechanisms influencing both myocardial and coronary function in hypertensive heart disease is the pressure-dependent development of smooth vascular hypertrophy (media) or coronary resistance vessels. Consequently, the oxygen supply to the myocardium is impaired and secondary lesions occur such as fibrosis, increased myocardial and perivascular collagen content and scars within the heart muscle. Diastolic dysfunction develops, as well as an increase in myocardial stiffness, thus promoting the transition from the concentric (compensated) to the eccentric or dilated (decompensated) state, with the consequence of the occurrence of cardiac failure. On the basis of both functional and morphological criteria, evidence is presented in this report that coronary small vessel disease is one of the underlying mechanism for the development of cardiac failure in hypertensive heart disease.
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PMID:Development of cardiac failure by coronary small vessel disease in hypertensive heart disease? 183 64

In order to establish morbidity and mortality in treated patients with essential hypertension, a prospective study was started in 1974. 714 patients were followed for 15 years. Admission criteria included diastolic blood pressure over 95 mmHg during one month on placebo, absence of malignant or accelerated hypertension and no recent (6 month) cardiovascular complication. According to target organ damage, 51% of patients were in WHO stage I, 35% in stage II and 14% in stage III. There were 342 males and 372 females, with mean age 58.7 +/- 9.8 years. Mean initial blood pressure was 181/110 +/- 12/8.9 mmHg. Treatment schedules included diuretics alone (23%), beta blockers alone (32%), diuretic and betablocker (38%), combined therapy with vasodilators (9%) and other forms of therapy (5%). 75 subjects failed to comply with therapy but were maintained in the analysis (intention to treat). A significant reduction in blood pressure was observed in the group as a whole (154/93 +/- 7/9 mmHg). Sustained normalization of BP (< 90 mmHg) was obtained in 40.2% of patients, reductions to between 91 and 100 mmHg in 37.2% and reductions to over 101 mmHg in 22.5% 47 patients died from cerebro vascular complications (15-year cumulative death rate of 12.3%). Total morbidity rate was 40.1% (232 events) with 61 coronary events (13.3%), 43 cerebrovascular events (8.7%), 30 cases of heart failure (12.9%) and 21 cases of renal failure (4.3%). These figures are in agreement with internationally reported ones with the exception of coronary morbidity which appears lower in this study.
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PMID:[Morbidity and mortality of essential arterial hypertension treated in Chile: a 15 years' follow-up study]. 184 49

To investigate the predisposing factors and the clinical significance of the musical aortic component of the second heart sound (musical S2), 18 patients with musical S2 (musical group) among the consecutive 2,000 patients with phonocardiographic examination were noninvasively studied by analyzing underlying diseases, phonocardiographic findings, organic changes of the aortic valve, severity of aortic regurgitation and left ventricular dysfunction. Organic changes of the aortic valve were assessed by two-dimensional echocardiography, and aortic regurgitation was assessed by color Doppler flow imaging. Twenty-two normal subjects (normal group) and 17 patients with essential hypertension (hypertensive group) served as controls. Mean ages were matched among the three groups. 1. Left ventricular dilatation (seven patients) and hypertension (six patients) were the dominant part of underlying disease in the musical group. 2. Musical S2 was classified in the following two types based on the phonocardiographic characteristics; musical vibrations followed immediately after the accentuated S2, and the S2 which was replaced by regular vibratory waves. 3. Frequency of the musical vibrations ranged from 120 to 200 Hz, and its duration ranged from 60 to 120 msec. Amplitude of the musical vibrations decreased by inhalation of amyl nitrite, but increased by infusion of methoxamine. In a case with mild rheumatic valve disease, methoxamine induced marked intensification of the amplitude and prolongation of the duration of the musical vibrations, finally giving a typical cooing murmur. 4. Echo intensity of the aortic valve tended to be higher in the musical group than in the other two groups. 5. Echocardiographically, aortic regurgitation appeared more frequently in the musical group (88%) than in the normal (36%) and hypertensive (41%) groups. Area of the aortic regurgitant signal was significantly larger in the musical group (4.1 +/- 1.4 cm2) than in the normal (1.2 +/- 0.8 cm2) and hypertensive (2.3 +/- 1.2 cm2) groups. 6. Left ventricular end-diastolic dimension was significantly larger in the musical group (5.8 +/- 0.6 cm) than in the normal (4.7 +/- 0.5 cm) and hypertensive (4.8 +/- 0.7 cm) groups. Fractional shortening of the left ventricle was significantly smaller in the musical group (26 +/- 10%) than in the normal (37 +/- 5%) and hypertensive (37 +/- 8%) groups. In a case of the musical group, musical vibrations following the S2, which was large in amplitude at the state of heart failure, decreased markedly after the recovery from heart failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Possible mechanism of production of the musical second heart sound and its clinical significance]. 188 56

Electrocardiographic signs of changes in the myocardium were detected in 93.2 percent of 74 patients with malignant maxillofacial tumors; this was due to the presence of coronary disease, myocardial dystrophy, essential hypertension, respiratory abnormalities. The development and progress of these shifts much depended on radiotherapy and chemoradiotherapy of the tumors. The most frequent findings were deviations in the end section of the ventricular complex, reflecting the metabolic and ischemic changes in the myocardium, associated with a rise in radiation and polychemotherapy dosage. Extracoronarogenic myocardial lesions and coronary disease progression were clinically characterized by augmentation of cardiac insufficiency and various arrhythmias with mild pain syndrome. These specific clinical and electrocardiographic features of myocardial involvement should be borne in mind when choosing and carrying out radio- and polychemoradiotherapy of patients with maxillofacial tumors.
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PMID:[The electrocardiographic changes in patients with malignant neoplasms of the maxillofacial area during radio- and chemotherapy]. 192 7

To document the clinical presentation of malignant accelerated hypertension in Nigerians, 56 patients were studied between 1987 and 1989 (30 months). Age range was 16 to 55 years with 59% in the range of 30-49 years; 47 were male. Mean systolic and diastolic blood pressures were 217 mmHg and 146 mmHg, respectively. Thirty patients had grade III and 26 grade IV hypertensive retinopathy. Mean body mass index was only 22.4 in the 21 patients who had no evidence of fluid retention. Seventy-five percent of patients had no awareness of hypertension. Essential hypertension accounted for 66%, chronic renal disease 32% and renal artery stenosis 2% of cases. The most common clinical features were headaches (80%), fatigue (68%), oliguria (52%), heart failure (46%), weight loss (41%), and poor vision (21%). Multiple symptoms were common and 24 patients had both renal and cardiac failure. Laboratory features included microscopic haematuria (100%) and proteinuria (100%). In 37 patients with essential hypertension, renal failure was a complication in 60%. Microangiopathic haemolytic anaemia was present in 23 patients. In addition to eight deaths from renal failure in the acute stage, 23 of these patients required long-term dialysis. Thus, malignant accelerated hypertension was associated with high morbidity, especially renal failure; it primarily afflicted patients in their prime years. Known survival at one year was 37.5%, but some patients were lost to follow-up.
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PMID:The clinical presentation of malignant hypertension in Nigerians. 195 31

Cardiac arrhythmias were studied in patients with essential hypertension in relation to their myocardial function. It was found that the arrhythmias occurring in the early period of the disease (borderline hypertension, Stage I hypertension) were primarily functional and affected the course of the disease and hemodynamics to a small degree. The life-threatening arrhythmias recorded in early hypertension were more commonly caused by mitral prolapse. The duration and severity of hypertension, development of left ventricular myocardial hypertrophy, myocardial fiber distension in relative heart failure play a decisive role in the development of cardiac arrhythmias in patients with Stage II hypertensive disease. It is essential to make comprehensive clinical and instrumental studies to clarify the genesis of the arrhythmic syndrome and to correctly choose the management policy in these patients.
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PMID:[Clinical significance of arrhythmia in patients with hypertension]. 206 87


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