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

Left ventricular hypertrophy (LVH) is a well defined cardiovascular risk factor and is frequently detected by echocardiography in hypertensive patients. Systolic cardiac function at rest is usually preserved in hypertension, however, diastolic function may be frequently altered. Evidence for these changes has been demonstrated by Echo-Doppler even without concomitant existence of LVH. Quantitative and qualitative changes in contractile proteins and interstitial tissue as well as reduction of coronary reserve may be related to the mentioned dysfunction. Recent studies have confirmed the precocity of diastolic dysfunction both in laboratory animals as well as man. Further significant differences have been shown between normotensives with and without a family history of systemic hypertension. The relative importance of diastolic disfunction is also related to its possible role in the genesis of cardiac failure and its probable role in the modulation of cardiopulmonary reflexes in addition to the hemodynamics of arterial hypertension. It is not yet known if the presence of diastolic dysfunction is a mechanism or a risk marker like LVH.
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PMID:[Precocity of diastolic dysfunction in hypertensive cardiopathy]. 138 59

Sixty million Americans have hypertension, a major cardiovascular risk factor. Its presence accelerates the atherosclerotic process, producing strokes, heart attacks, heart failure, renal failure, and peripheral vascular disease. This article highlights the historical landmarks in the study of this disease from the first documented measurement of blood pressure in 1733, through the most recent pharmacologic approaches to treatment. In addition, the roles of the kidney and the renin-angiotensin-aldosterone system are examined.
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PMID:Historical reflections on hypertension. 194 83

The hypertensive cardiopathy is a controversial entity as regards the physiopathological mechanisms and clinical aspects. Defined as the hypertrophy of the left ventricle, secondary to the permanent tension increases, it accompanies not only the severe forms of arterial hypertension but also the medium and mild ones. In the authors' opinion, based on numerous experimental and clinical studies, the main factor that initiates the myocardial hypertrophy is the increased parietal tension (hemodynamic hypertrophy). The natural evolution is progressive, the myocardial hypertrophy initially adaptive becomes pathological and the cardiac performance is affected gradually, first in its diastolic and then in its systolic component, up to the final stage of congestive cardiac insufficiency. The structural changes of the myocardial fibre also document the adaptive and pathological hypertrophy, the alteration of the myocardial contractility consisting in the difficulty of transforming the chemical energy into mechanical work. The clinical aspects show an incipient myocardial hypertrophy, considered adaptive, since the cardiac performance is normal; an important hypertrophy affecting the diastolic component and the hypertrophy with dilatation that affects the overall performance. Of the evaluation methods, the echocardiography is the most accurate one in quantifying hypertrophy, evaluation of the cardiac performance and possibility of detecting several characteristic aspects of the hypertensive cardiopathy. The transition moment from the adaptive hypertrophy to the pathological hypertrophy cannot be exactly established but it is documented that the hemodynamic and nonhemodynamic hypertrophy is a supplementary cardiovascular risk factor.
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PMID:[Hypertensive cardiopathy--an adaptive or a pathologic phenomenon?]. 257 41

Our understanding of left ventricular hypertrophy has increased considerably in recent years with the introduction of new investigative techniques and the publication of clinical and epidemiological studies. The mechanism of the genesis of LVH is complex and multifactorial: besides the purely mechanical explanation which places LVH in a purely compensatory complex, counteracting the increase in left ventricular load, many other factors have been incriminated including a genetic predisposition and neurohormonal activation. A long phase of compensation is followed by ventricular insufficiency and cardiac failure. In addition, LVH has been identified as an independent cardiovascular risk factor for increased morbidity and mortality. Partial regression of LVH after surgical correction of valvular disease and especially after treatment with certain antihypertensive drugs, should be considered with great interest, even though the long-term prognosis of this regression remains uncertain.
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PMID:[Left ventricular hypertrophy: a real compensatory mechanism?]. 821 84

Hypertension is an important cardiovascular risk factor. High blood pressure per se is not a disease but a hemodynamic alteration associated with vascular disease. Two classes of drugs are especially effective in lowering blood pressure and preventing cardiovascular complications, angiotensin converting enzyme (ACE) inhibitors and calcium antagonists. The hemodynamic effects of ACE inhibitors and calcium antagonists are complementary. While ACE inhibitors inhibit the renin-angiotensin system and reduce sympathetic outflow, calcium antagonists dilate large conduit and resistance arteries. Certain calcium antagonists, such as verapamil, lower heart rate. In the blood vessel wall, the local vascular effects of ACE inhibitors and calcium antagonists are also complementary. While ACE inhibitors inhibit activation of angiotensin I into angiotensin II and prevent the breakdown of bradykinin (which stimulates nitric oxide and prostacyclin formation), calcium antagonists inhibit the effects of vasoconstrictor hormones such as angiotensin II at the level of vascular smooth muscle by reducing calcium inflow and facilitating the vasodilator effects of nitric oxide. Calcium antagonists reduce smooth muscle cell proliferation and atherosclerosis. In hypertensive animals, verapamil and trandolapril normalize endothelial dysfunction. In large angiographic trials, nifedipine and nicardipine reduced the development of new atherosclerotic plaques. After myocardial infarction, verapamil reduces mortality and cardiac events in patients without heart failure. In contrast, ACE inhibitors are effective after myocardial infarction in patients with impaired left ventricular function. Urinary albumin excretion rate decreases during ACE inhibitor therapy or with a calcium antagonist such as verapamil; combination of the two drugs has an additive effect. In resistance arteries, hypertension is associated with an increased media/lumen ratio. ACE inhibitors, but not beta-blockers, markedly improve these structural changes. In summary, ACE inhibitors and calcium antagonists have a complementary profile, both in their hemodynamic and local vascular action. Hence, combination therapy with these two classes of drugs appears particularly useful in patients with hypertension, not only to lower blood pressure, but hopefully to achieve improved cardiovascular protection.
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PMID:Vascular protective effects of ACE inhibitors and calcium antagonists: theoretical basis for a combination therapy in hypertension and other cardiovascular diseases. 856 68

The objective of the study is to compare fatal and nonfatal cardiovascular endpoints in hypertensive patients randomised to the calcium-channel blocker, nifedipine GITS or a thiazide diuretic, co-amilozide. A total of 6592 patients from nine countries (UK, France, Israel, Spain, Italy, The Netherlands, Sweden, Denmark and Norway) will be recruited, aged 55-80 and with a blood pressure (BP) > or = 150/95 or > or = 160 mm Hg (systolic). All patients will have at least one other major cardiovascular risk factor. Patients will be minimised by country and risk factors and randomised to double-blind treatment with either nifedipine GITS or diuretic. After a single dose titration, additional treatment will be atenolol or enalapril (where beta-blockade is contra-indicated). After achieving a target BP of 140/90 mm Hg patients will be followed for a total of 3 years. Primary endpoints are myocardial infarction, stroke, subarachnoid haemorrhage, heart failure and sudden cardiac death. The study has a power of 80% at 5% significance to detect a difference between 8% event rate over 3 years in diuretic-treated patients and 6% in those receiving nifedipine.
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PMID:INSIGHT: international nifedipine GITS study intervention as a goal in hypertension treatment. 887 50

Accumulating evidence suggests from experimental and clinical studies beneficial effects of growth hormone (GH) on contractility, although concomitant cardiac hypertrophy, generally considered to be a cardiovascular risk factor, has also been reported. In the present study, we combine a rat model with impaired cardiac performance after myocardial infarction (MI) with echocardiographic evaluation of GH effects on cardiac structure and function. We have used a rat model with ligation of the left coronary artery in normal, growing male rats resulting in subsequent impaired cardiac performance. After 6 weeks' recovery, blind transthoracic echocardiography was performed to determine infarction size, cardiac geometry and performance. Rats with no signs of myocardial infarction were excluded from the study. After randomization, the rats were treated with daily s.c. injections of saline (n = 8) or recombinant human growth hormone (rhGH) (n = 6) at a dose of approximately 1 mg kg-1 body weight for 1 week. A new blind echocardiography examination was performed after treatment demonstrating a 13% increase in ejection fraction (EF) and a 50% increase in cardiac index in GH-treated rats compared with control rats (P < 0.01). Moreover, GH caused a significant decrease in end-systolic volume. There were no significant changes in left ventricular (LV) or interventricular wall thickness, LV dimensions, heart rate or diastolic function. No effects were seen on LV weight, cardiac insulin-like growth factor (IGF) I, IGF-I receptor and GH receptor mRNA content. GH in a physiological dose improves systolic function in an experimental model of heart failure without signs of hypertrophy, suggesting a potential role as a therapeutic agent in the treatment of heart failure and merits further investigation.
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PMID:Growth hormone improves cardiac function in rats with experimental myocardial infarction. 922 33

The variable prognosis after myocardial infarction necessitates an individual tailoring of follow-up treatment. Therapeutic decisions must be based on a complete risk stratification including assessment of persisting ischemia, left ventricular function, rhythmic instability and cardiovascular risk factor profile. High risk patients (prognostic indication) as well as symptomatic patients (symptomatic indication) should be referred for coronary angiography to assess the need for revascularisation procedures (PTCA, CABG). The individual risk profile also defines drug therapy for secondary prevention (not more than 3-4 drugs): anti-platelet agents or anticoagulation in every patient; beta blockers in all but the lowest risk group; ACE-inhibitors in heart failure or asymptomatic, substantial left ventricular dysfunction; liberal use of cholesterol-reducing drugs. Life style alterations should be encouraged in almost every patient. Information about the necessary measures to be taken upon occurrence of angina at rest or other cardiac symptoms must be repeatedly given to all patients.
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PMID:[After care of acute myocardial infarct: what are the 4 most important points?]. 932 21

Hypertension is a very important cardiovascular risk factor and directly leads to major atherosclerotic cardiovascular diseases, including coronary artery disease, stroke cardiac failure and peripheral artery disease. Hypertension tends to cluster with other atherogenic risk factors like dyslipidemia, insulin resistance, obesity and others. The association between hypertension and dyslipidemia is very frequent and the risk is more than additive and its possible pathogenesis may be of a common mechanism. Insulin resistance is the main cause of both risk factors. Endothelium dysfunction is present in arterial hypertension and dyslipidemia and the pathogenesis of atherosclerosis. The treatment of hypertensive patients must be individualized to accommodate both the concomitant dyslipidemia and other atherogenic factors.
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PMID:[Hypertension and dyslipidemia]. 988 66

Arterial hypertension (HBP) is a very important cardiovascular risk factor. According to the data from the Framingham Study, 90% of the patients with chronic heart failure (CHF) have a clinical history of HBP, and the risk of developing CHF is 2 to 3 times greater in hypertensive persons. Studies of general population by multivariate analysis have shown that HBP is responsible for 39% of CHF cases in males and 59% in females. On the other hand, there is a significant relation between HBP and coronary artery disease (CAD), another very important cause of CHF. HBP very frequently originates left ventricular hypertrophy (LVH) and this is one of the most important links between HBP, myocardium ischaemia, CAD, and sudden death from arrhythmias, to which it can lead. Recent studies on left ventricle systolic function in hypertensive patients indicate that about 1/6 of HBP patients with LVH present systolic dysfunction. Even more frequently, diastolic function is prematurely deteriorated in HBP. In spite of the existence of a significant relation between the grade of LVH and the severity of this disfunction, it may be present even before LVH is detectable. The transition from LVH would be related to quantitative and qualitative changes in the three compartments of the myocardium: hypertrophy of cardiomyocytes with reinduction of fetal genetic program, reactive and cicatricial fibrosis of the interstice, and functional and structural changes of coronary arteries. These modifications will progressively increase, leading to LV dilation which seems to signal transition to heart failure. In recent papers the transition from LVH to CHF has been related to a marked increase in microtubular intracytoplasmic structure, the reduction of Ca++ ATPase concentration of the sarcoplasmic reticulum, and the increased myocardial expression of growth factor TGF beta 1, which influences interstitial fibrosis. In the same way, stimulation of apoptosis by myocardial expression of tumor necrosis factor alpha and the subquent increase in inducible NO-synthase and oxidative stress has been related to the progression for CHF. Prevention of CHF will not only consist in the treatment of HBP but, very probably, also in the prevention of regression of LVH, and normalization of myocardial components, as well as the correction of all the factors involved in CHF establishment. In accordance with form of treatment, we must give special emphasis to drugs interfering with the renin-angiotensin system and, possibly in the near future, to gene therapy.
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PMID:[Hypertensive cardiopathy. From arterial hypertension to congestive heart failure]. 1042 61


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