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Biomedical subjects

F H Messerli

Publications and source records attributed to F H Messerli.

At least 235 records · Page 13Linked to original sources
PubMed1986

Immediate and short-term hemodynamic effects of diltiazem in patients with hypertension.

The immediate effects of intravenous diltiazem effects and short-term (4 weeks) of the oral drug on systemic and regional hemodynamics, cardiac structure, and humoral responses were evaluated by previously reported methods in nine patients with mild-to-moderate essential hypertension and in one patient with primary aldosteronism. Diltiazem was first administered in three intravenous doses of 0.06, 0.06, and 0.12 mg/kg, respectively; patients were then treated for 4 weeks with daily doses ranging from 240 to 360 mg (average 300 mg). Intravenous diltiazem immediately reduced mean arterial pressure (from 115 +/- 3 to 96 +/- 3 mm Hg; p less than .01) through a fall in total peripheral resistance index (from 37 +/- 3 to 23 +/- 2 U/m2; p less than .01) that was associated with an increase in heart rate (from 66 +/- 2 to 77 +/- 3 beats/min; p less than .01) and cardiac index (from 3.3 +/- 0.3 to 4.3 +/- 0.4 liters/min/m2; p less than .01). These changes were not associated with changes in plasma levels of catecholamines or aldosterone or in plasma renin activity. After 4 weeks the significant decrease in mean arterial pressure persisted (104 +/- 3 mm Hg; p less than .01) and there were still no changes in the humoral substances or plasma volume. Renal blood flow index increased (from 368 +/- 52 to 462 +/- 57 ml/min/m2; p less than .01) and renal vascular resistance index decreased (from 0.37 +/- 0.06 to 0.26 +/- 0.04 U/m2; p less than .01), while splanchnic hemodynamics did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Cardiovascular adaptation to obesity and hypertension.

Hypertension and obesity are two disorders that are closely related; each occurs more frequently with the other than in an otherwise normal population. These two disorders, however, exert disparate effects on cardiovascular structure and function. The hallmark of essential hypertension is an increased total peripheral resistance, and hypertensive patients have a contracted intravascular volume and normal cardiac output but an increased left ventricular stroke work due to a high afterload. In contrast, obese patients have an increased intravascular volume, left ventricular filling pressure, cardiac output and a lower total peripheral and renal vascular resistance. Left ventricular adaptation will consist of eccentric hypertrophy in obesity regardless of the level of arterial pressure and concentric hypertrophy in lean hypertensive patients. Although obesity may mitigate the harmful effect of a chronically elevated total peripheral and renal vascular resistance and lessen target organ damage in essential hypertension, the combination of obesity and hypertension presents a double burden to the left ventricle and is associated with systolic and diastolic dysfunction and a propensity for high grade ventricular dysrhythmias. It is not surprising that congestive heart failure and sudden death are common sequelae of obesity hypertension. Weight reduction reduces arterial pressure by decreasing intravascular volume and cardiac output associated with a fall in sympathetic activity and reversal of cardiac hypertrophy. Therefore, weight loss unloads the heart from the two-fold burden caused by obesity and hypertension and should become a major goal in the prevention and treatment of heart disease.

Arrhythmias, Cardiac↗
PubMed1986

Left ventricular hypertrophy. A cardiovascular risk factor in essential hypertension.

The heart adapts to increasing afterload, such as that which occurs in arterial hypertension, with an increase in wall thickness in order to bring wall stress back to normal. As a consequence, concentric left ventricular hypertrophy ensues. Hypertension as well as advancing age has been shown to be associated with an increase in posterior wall thickness. Accordingly, the prevalence of left ventricular hypertrophy becomes very high in the elderly and may occur in more than 50% of elderly hypertensive patients. Left ventricular hypertrophy is not merely a physiological process serving to compensate for the increased afterload. The Framingham study has indicated that patients with left ventricular hypertrophy are at an increased risk of sudden death and other cardiovascular morbidity and mortality. The risk for sudden death is 5 to 6 times higher in patients with left ventricular hypertrophy than in those without, regardless of levels of arterial pressure. By Holter monitoring of these patients it has been shown that those with left ventricular hypertrophy have a prevalence of premature ventricular contractions that is 40 to 50 times higher than those patients without left ventricular hypertrophy. In addition, patients with left ventricular hypertrophy rated substantially higher with regard to Lown's classes than those without. These data indicate that left ventricular hypertrophy is common, particularly in the elderly, and predisposes to ventricular ectopy, higher grade arrhythmias, and sudden death. Clearly, these considerations have to be taken into account when selecting antihypertensive therapy inasmuch as hypokalaemia, hypomagnesaemia, and other electrolyte shifts predisposing to ventricular arrhythmias must be scrupulously avoided.

Age Factors↗
PubMed1986

Renal involvement follows cardiac enlargement in essential hypertension.

To assess the relationship between early clinically detectable involvement of hypertensive vascular disease in heart and kidneys, we obtained systemic and renal hemodynamic and M-mode echocardiographic measurements in 65 patients with essential hypertension. The results indicate that patients with and without left ventricular hypertrophy had similar renal hemodynamic findings. In contrast, patients with altered renal hemodynamic measurements (ie, reduced renal distribution of cardiac output and, therefore, absolute renal blood flow with increased renal vascular resistance) and increased serum uric acid levels also had increased left ventricular posterior and septal wall thicknesses and mass index. Moreover, these data also demonstrated that in patients with altered renal hemodynamics, the lower the renal distribution of cardiac output and the higher the serum uric acid levels, the greater were the indexes of cardiac enlargement. These results demonstrated that the pathophysiological and hemodynamic effects of essential hypertension in the heart precede those in the kidneys.

Adult↗
PubMed1986

Risks for obesity.

Whether or not obesity per se is an independent risk factor remains controversial. However, a variety of studies have shown that obesity precipitates certain well-known risk factors, such as glucose intolerance, hyperlipidemia, hyperestrogenemia, hypertension, and left ventricular hypertrophy. Distribution of adipose tissue also seems to influence cardiovascular risk; patients with predominantly male-pattern obesity exhibit more profound risk for cardiovascular disease.

Blood Glucose↗
PubMed1986

Pathophysiology of hypertension in the elderly.

Combined systolic and diastolic arterial hypertension and isolated systolic hypertension in the elderly are proven risk factors for stroke, sudden death, coronary artery disease, and congestive heart failure. Because hemodynamics, vascular and cardiac adaptations, fluid volume, and endocrine functions are distinctly altered in the elderly hypertensive patient compared with a younger patient, antihypertensive treatment should be individualized, and an unsophisticated regimen, such as a stepped-care approach, is too rigid to be as beneficial for elderly hypertensive patients as for young hypertensive patients.

Aged↗
PubMed1986

Risks for arterial hypertension.

In this article, the most important risk factors that may predict the transition from borderline to established hypertension are reviewed. Primary prevention has to focus on identifying individuals who are at highest risk and delaying or reversing further elevation of arterial pressure levels. A review of the literature indicates that several environmental and congenital factors can be identified as risk factors for the development of hypertension, including family history of essential hypertension, age, race, obesity, alcohol consumption, salt intake, hormonal status, and some stress factors. Of all diagnostic approaches to predict the development of hypertension, measurements of resting heart rate and responses to dynamic exercise have some predictive value.

Adult↗
PubMed1985

Osler's maneuver and pseudohypertension.

We describe a simple bedside procedure (which we call "Osler's maneuver") that differentiates patients with true hypertension from those whose blood pressure is spuriously elevated because of excessive sclerosis of the large arteries ("pseudohypertension"). The maneuver is performed by assessing the palpability of the pulseless radial or brachial artery distal to a point of occlusion of the artery manually or by cuff pressure. We classified 24 elderly hypertensive patients as either Osler-positive (n = 13) or Osler-negative (n = 11), and measured their intraarterial pressure, arterial compliance, and systemic hemodynamics. Patients with pseudohypertension (Osler-positive) had falsely elevated blood-pressure readings, with a difference of 10 to 54 mm Hg between cuff and intraarterial pressure. Arterial compliance was lower in Osler-positive subjects and correlated with the difference between cuff and intraarterial pressures, indicating that the stiffer the artery, the more pronounced the degree of pseudohypertension. Pseudohypertension is common in the elderly and becomes more severe as arterial compliance decreases and sclerosis of large arteries progresses.

Aged↗
PubMed1985

Cardiovascular effects and regional blood flow distribution associated with angiotensin converting enzyme inhibition (captopril) in essential hypertension.

Systemic and regional hemodynamics and cardiac structural changes were studied in 12 patients with mild to moderately severe essential hypertension before and then 90 minutes and 12 weeks after administration of captopril. Mean arterial pressure was reduced from 111 mm Hg to 96 mm Hg (p less than 0.001), and this was mediated through a fall in total peripheral resistance from 26 +/- 2 units to 23 +/- 2 units (p less than 0.01). The decreased total peripheral resistance was distributed to all circulations studied: kidney, skeletal muscle, skin and the splanchnic organs. Furthermore, left ventricular (LV) mass index diminished without altering myocardial contractility at rest. Thus, captopril lowered arterial pressure through systemic arteriolar dilatation in patients with mild to moderately severe essential hypertension and also reduced LV mass even in patients without evidence of LV hypertrophy.

Adult↗
PubMed1985

Immediate hemodynamic effects of urapidil in patients with essential hypertension.

Systemic, renal and splanchnic hemodynamics and certain reflex and endocrine responses were determined in 10 patients with essential hypertension before and after intravenous administration of urapidil, a new antihypertensive agent that acts through both central and peripheral alpha-adrenergic inhibitory mechanisms. The reduction in mean arterial pressure by 12% (103 +/- 3 vs 91 +/- 6 mm Hg, p less than 0.05) was mediated through a decreased total peripheral resistance index (from 34 +/- 2 to 25 +/- 3 U/m2, p less than 0.01), which was associated with a significant reflexive increase in cardiac index, heart rate and serum norepinephrine level. This hypotensive effect was also associated with blunted Valsalva overshoot and orthostatic hypotension, suggesting peripheral arteriolar and venular dilation. Renal and splanchnic blood flows increased (p less than 0.05), resistances in these vascular beds decreased (p less than 0.01) and there were no changes in creatinine clearance or glomerular filtration fraction. Thus, intravenous urapidil reduced arterial pressure by decreasing total peripheral, renal and splanchnic resistances associated with maintained organ flows and increased heart rate and cardiac index.

Antihypertensive Agents↗
PubMed1985

Arterial compliance in essential hypertension.

Arterial compliance as evaluated by three different indices (pulse wave velocity, pulse pressure stroke volume, and an exponential analysis of the diastolic pressure decay) was found to be abnormal in patients with established essential hypertension and particularly in elderly hypertensive patients. Two of the three indices reflected significantly impaired arterial compliance already in borderline hypertension. Age, systolic, and diastolic pressures evolved as independent determinants of pulse wave velocity. It is concluded that arterial compliance becomes impaired early in hypertensive cardiovascular disease at the time when arterial pressure is only to the borderline level. However, age per se seems to be the most predominant risk factor for systemic arterial disease.

Adult↗
PubMed1985

Cardiovascular pathophysiology of essential hypertension: a clue to therapy.

Arterial hypertension is by definition a haemodynamic disorder. At least 3 different subsets of cardiovascular pathophysiological features can be identified in so-called essential hypertension: The young lean patient characterised by an elevated cardiac output and renal blood flow, elevated plasma renin activity and circulating catecholamine levels, as well as symptoms and signs of hyperadrenergic hypertension. The elderly patient characterised by a low cardiac output often with left ventricular hypertrophy, elevated total peripheral resistance, nephrosclerosis, and symptoms and signs of target organ disease. The obese patient (and to a lesser degree the black patient) characterised by expanded fluid volume state, elevated cardiac output, a normal to low total peripheral resistance, and symptoms and signs of volume overload. To initiate antihypertensive therapy, the drug of choice in the young patient is a beta-adrenergic receptor blocker; in the elderly it is a haemodynamic vasodilator (anti-adrenergic drug, slow channel calcium blocker, or converting enzyme (ACE) inhibitor), and in black or obese patients it remains a thiazide diuretic. Enalapril, a new ACE inhibitor is indicated as a first-step agent in the great majority of hypertensive patients in whom the elevated arterial pressure should be reduced by a decrease in total peripheral resistance, without compromising systemic or regional blood flow. In contrast to other antihypertensive agents, enalapril will lower preload and afterload to the left ventricle while improving systemic and regional flow in elderly patients with latent or manifest congestive heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1985

Hemodynamic and cardiac adaptation in essential hypertension. Consequences for therapy.

In so-called essential hypertension, at least three different subsets of pathophysiologic findings can be identified: mild hypertension in nonobese juvenile subjects characterized by elevated cardiac output, normal peripheral resistance, increased sympathetic activity as measured by norepinephrine and plasma renin activity; hypertension in the elderly with a low cardiac output, often with left ventricular hypertrophy, elevated total peripheral resistance, nephrosclerosis contracted intravascular volume, and low plasma renin activity; and obese hypertensive patients with a high cardiac output, expanded intravascular volume, and a normal total peripheral resistance. Although there is often an overlap among these three entities, antihypertensive treatment can easily be adapted accordingly. A beta-adrenoreceptor blocker is the step-one drug to be used in mild hypertension with an elevated cardiac output. The drug's negative inotropic and chronotropic properties will bring the elevated cardiac output and heart rate back to normal. In the elderly hypertensive patient, an arteriolar and venous vasodilator, such as an antiadrenergic agent, slow channel calcium blocker, or a converting enzyme inhibitor, will lower total peripheral resistance and unburden the left ventricle. In the obese patient and also in most black subjects, the first-step antihypertensive agent remains a thiazide diuretic. Labetalol, an agent with both beta- and alpha-adrenoreceptor properties, shows promise for the treatment of hypertension in the young as well as in the older patient. It seems to be the agent of choice in patients with established essential hypertension who are concomitantly suffering from coronary artery disease.

Adaptation, Physiological↗
PubMed1985

Disparate cardiac effects of afterload reduction in hypertension.

Cardiac performance, as judged by preload, afterload, and myocardial contractility, was evaluated by non-invasive M-mode echocardiography before and after acute oral administration of calcium entry blockers (nitrendipine and verapamil), angiotensin converting enzyme (ACE) inhibitors (captopril and lisinopril), and a dopamine receptor agonist (fenoldopam) in patients with mild to moderate essential hypertension. Left ventricular end diastolic volume was taken as an index of preload, end systolic stress as an index of afterload, and the ratio of systolic pressure to end systolic volume (SBP:ESV), ejection fraction (EF), and mean velocity of circumferential fibre shortening (Vcf) as indices of contractility. Reductions of afterload and mean arterial pressure were achieved with all antihypertensive agents involved (mean percentage change +/- s.e.m.: 15 +/- 2% and 10 +/- 1%, respectively, P < 0.05) but the afterload reduction with lisinopril was greatest (21 +/- 9%; P < 0.01). The dopamine receptor agonist fenoldopam decreased by preload 24% (P < 0.05) and increased all of the three parameters of myocardial contractility (SBP:SV 66%; EF 17%, Vcf 19%; P < 0.01). In contrast, no effect on these parameters was observed with either calcium entry blocker or either ACE inhibitor.

Adult↗
PubMed1984

Immediate regional blood flow distribution following angiotensin converting enzyme inhibition in patients with essential hypertension.

The increased total peripheral resistance that characterizes essential hypertension is generally reversed by antihypertensive drugs, but the reduction may not be uniform in all regions of the body. In this study, regional blood flow was investigated immediately after the oral administration of 25 mg of captopril in 11 patients with mild to moderate essential hypertension. Within 90 minutes, the total vascular resistance decreased significantly, and the decrease was significant in the kidney. It decreased but not significantly in the splanchnic organs, the skeletal musculature, and the skin. In no region was the blood flow reduced. As captopril has no direct effect on smooth muscle, these effects are likely to have been due to angiotensin converting enzyme inhibition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Enalapril improves systemic and renal hemodynamics and allows regression of left ventricular mass in essential hypertension.

Enalapril, a new angiotensin-converting enzyme inhibitor, is an effective antihypertensive agent for both renovascular and essential hypertension. It is structurally different from captopril in that it does not possess a sulfhydryl group. The systemic and renal hemodynamic, biochemical and cardiac adaptive changes induced by enalapril were studied in 8 patients with essential hypertension before and after 12 weeks of therapy. Mean arterial pressure decreased from 110 to 90 mm Hg (p less than 0.01), and this was mediated through a decrease in total peripheral resistance from 42 +/- 3 to 32 +/- 3 U (p less than 0.01). Cardiac index and heart rate did not change. Renal plasma flow was increased in 6 of 8 patients and renal vascular resistance decreased from 123 +/- 6 to 91 +/- 7 U (p less than 0.001). Left ventricular mass index decreased from a mean of 166 +/- 29 to 117 +/- 8 g/m2 (p less than 0.05) without impaired myocardial contractility. Thus, enalapril lowers arterial pressure by reducing total peripheral resistance without reflexive cardiac effects. It also has favorable hemodynamic effects on the kidney. This is the first report of regression of LV mass with this agent in man.

Adult↗