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Biomedical subjects

J Grimm

Publications and source records attributed to J Grimm.

At least 109 records · Page 6Linked to original sources
PubMed1984

[A new thermodilution catheter for the determination of heart-minute volume in the arterial system].

A double-lumen polyethylene pigtail catheter (F8, length 100 cm) for the determination of cardiac output (CO) in the arterial system is described. Following femoral insertion of the catheter, 10 ml of ice-cold saline is injected into the left ventricle through the distally ending lumen (0.8 mm2). Through the second lumen (0.8 mm2) which opens 50 cm behind the catheter tip, a thermistor probe (F3, teflon) is advanced into the descending aorta for recording of thermodilution curves. In 21 patients CO was determined first by the Fick method and then by thermodilution in the arterial system. CO by thermodilution correlated favorably with CO by Fick (r = 0.92, SEE 518 ml = 11% of the mean value). There was no systematic deviation from the reference CO. A similarly good correlation existed between stroke volume (SV) by thermodilution and SV by Fick (r = 0.86 SEE 11 ml = 15% of the mean value). Heart rate during thermodilution was 71 bpm, during Fick output estimation 72 bpm (not significant). Following withdrawal of the thermistor probe, simultaneous measurements of left ventricular and aortic pressures can be performed.

Cardiac Catheterization↗
PubMed1984

Diastolic stiffness and myocardial structure in aortic valve disease before and after valve replacement.

Passive diastolic properties were determined in 10 control patients and 21 patients with aortic valve disease before and 17.5 months after successful valve replacement. Ten patients had severe aortic stenoses (AS), five had combined aortic valve lesions (AS + aortic insufficiency [AI]), and six patients had severe AI. Left ventricular endomyocardial biopsies were obtained before and after surgery in patients with AS, AS + AI, and AI. Simultaneous echocardiographic and high-fidelity pressure measurements were made in all patients, and left ventricular chamber stiffness was calculated from a viscoelastic pressure-circumference relationship and left ventricular myocardial stiffness from a viscoelastic stress-strain relationship. The constant of chamber stiffness, beta', was slightly although not significantly increased in patients with AS (0.27 before and 0.24 after surgery), but was normal in those with AS + AI (0.22 before and 0.17 after surgery) and slightly decreased in those with AI (0.18 before and 0.16 after surgery) when compared with in control subjects (0.21). The constant of myocardial stiffness beta was normal in patients with AS (13.2), AS + AI (11.5), and AI (11.7) before surgery compared with in the control group (12.5). beta increased, however, significantly in those with AS (25.2; p less than .02), but not in those with AS + AI (16.3; NS) and AI (12.8; NS) after surgery. Myocardial morphologic characteristics showed a significant decrease in muscle fiber diameter in patients with AS, AS + AI, and AI, as well as a significant increase in interstitial fibrosis from 15% to 26% (p less than .05) in those with AS and a slight increase from 15% to 22% (NS) in those with AS + AI and from 19% to 24% (NS) in those with AI. Left ventricular fibrous content (left ventricular muscle mass index multiplied by interstitial fibrosis) remained, however, unchanged in all three groups after aortic valve replacement. In conclusion, left ventricular chamber stiffness is increased in AS but decreased in AI, whereas LV myocardial stiffness is normal in patients with aortic valve disease before surgery. After surgery, left ventricular myocardial stiffness increased significantly in AS patients but remained unchanged in those with AI. Postoperative changes in myocardial structure were characterized by a decrease in muscle fiber diameter and a relative increase in interstitial fibrosis, whereas fibrous content remained unchanged. Thus, regression of myocardial hypertrophy in aortic valve disease is accompanied by an increase of myocardial stiffness in concentric hypertrophy that is not seen in eccentric hypertrophy.

Adult↗
PubMed1984

Diastolic function in aortic valve disease: techniques of evaluation and pre-/postoperative changes.

Passive diastolic properties of the left ventricle are determined by several factors intrinsic or extrinsic to the ventricle. In patients with myocardial hypertrophy due to longstanding pressure or volume overload increased muscle mass and structural alterations of the myocardium are responsible for changes in passive elastic properties. Evaluation of diastolic function includes determination of ventricular (= chamber) and myocardial (= muscle) stiffness from simultaneous pressure-volume and stress-strain relations during passive diastolic filling. The slope of the pressure-volume relationship is equal to the constant of chamber stiffness and the slope of the stress-strain relationship equal to the constant of myocardial stiffness. Passive diastolic properties were determined in ten control patients and 21 patients with aortic valve disease before and 17.5 months after successful valve replacement. Ten patients presented with severe aortic stenosis, five patients with combined valve lesions and six patients with severe aortic insufficiency. Simultaneous high-fidelity pressure measurements and M-mode echocardiography were carried out in all patients. Myocardial stiffness was calculated from a viscoelastic stress-strain relationship using a nonlinear curve-fit program. Standard hemodynamic measurements showed a significant decrease in pressure and volume overload after successful valve replacement. Left ventricular muscle mass index decreased in all three groups significantly after surgery, whereas systolic ejection fraction remained unchanged pre-/postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Stenosis, Subvalvular↗
PubMed1984

[Relaxation and regional myocardial stiffness in obstructive hypertrophic cardiopathy patients: effect of verapamil].

Diastolic stiffness of the septum and the posterior wall were determined in 6 patients with hypertrophic obstructive cardiomyopathy before and 10 to 15 min after the intravenous administration of verapamil, 0,1 mg/kg. Left ventricular high-fidelity pressure measurements and M-mode echocardiography were carried out in all patients before and after verapamil. Diastolic stiffness of the septum (beta S) and of the posterior wall (beta) were assessed from the slope of a viscoelastic stress-strain relationship: sigma = alpha (e beta epsilon -1) + eta epsilon where sigma = meridional wall stress (g/cm2) alpha = intercept (g/cm2), beta = constant of myocardial stiffness, epsilon = mid-wall strain, eta = constant of myocardial viscosity (g. sec/cm2), epsilon = strain rate (sec-1). Left ventricular relaxation was evaluated from the time constant of left ventricular pressure fall (T; msec) by plotting left ventricular pressure versus dP/dt during the isovolumic relaxation period. Heart rate (71 versus 74 beats/min), left ventricular end-diastolic pressure (17 versus 17 mmHg) and peak systolic pressure (152 versus 146 mmHg) were not significantly different before and after intravenous administration of verapamil. The constant of myocardial wall stiffness of the septum (17 versus 16) and the posterior wall (15 versus 13) remained unchanged after verapamil, however, myocardial stiffness of the septum was slightly higher than myocardial stiffness of the posterior wall. The time constant of left ventricular pressure fall decreased significantly (P less than 0.05) from 53 to 43 msec following administration of verapamil. It is concluded that in patients with hypertrophic, obstructive cardiomyopathy, diastolic myocardial stiffness of the septum is slightly higher than the stiffness of the posterior wall. Verapamil does not influence the regional passive diastolic properties but has a beneficial effect on ventricular relaxation.

Blood Pressure↗
PubMed1983

Diastolic function in hypertrophic cardiomyopathy: effects of propranolol and verapamil on diastolic stiffness.

In patients with hypertrophic cardiomyopathy (HCM), impaired left ventricular (LV) relaxation and diastolic filling have been reported. Therefore, we determined LV diastolic stiffness in nine patients with HCM before and 10 to 15 min after 0.15 mg/kg propranolol i.v. (group 1) and in six patients with HCM before and 10 to 15 min after 0.1 mg/kg verapamil i.v. (group 2). Simultaneous LV cineangiography and high-fidelity pressure measurements were performed in group 1 and simultaneous M-mode echocardiography and high-fidelity pressure measurements in group 2. Passive LV chamber stiffness was determined in group 1 from the diastolic pressure-volume data using an exponential three-parameter model: P = ae beta V + C, where P = pressure, alpha = intercept, beta = constant of chamber stiffness, V = volume and C = baseline pressure. Passive LV myocardial stiffness was estimated in group 2 from the diastolic stress-strain data using a viscoelastic model: sigma = alpha' (e beta' epsilon -1) + eta epsilon, where sigma = meridional wall stress, alpha = intercept, beta' = constant of myocardial stiffness, epsilon = midwall strain, eta = constant of myocardial viscosity and epsilon = strain rate. LV relaxation was assessed from the time constant of LV pressure decay (T) by plotting LV pressure versus negative dP/dt. LV diastolic filling was evaluated from peak and mean LV filling rate in group 1 and from peak and mean midwall lengthening rate in group 2. LV chamber and myocardial stiffness, respectively, remained unchanged before and after administration of propranolol (beta = 0.054 and 0.047) and verapamil (beta' = 14.8 and 12.6); however, the time constant of LV pressure decay T increased significantly in group 1 from 45 to 66 ms (P less than 0.05) and decreased significantly in group 2 from 53 to 43 ms (P less than 0.05). Parallel to the changes in LV isovolumic relaxation, mean LV diastolic filling rate decreased significantly in group 1 from 257 to 196 ml m-2 s-1 (P less than 0.025) and mean LV midwall lengthening rate increased significantly in group 2 from 2.37 to 4.31 cm/sec (P less than 0.05). It is concluded that LV diastolic stiffness remains unchanged in patients with HCM after propranolol and verapamil. LV relaxation and mean diastolic filling, however, are impaired in patients with HCM following propranolol but are improved after verapamil. Thus, the beneficial effect of verapamil on diastolic mechanics is related to improved relaxation and diastolic filling rather than to changes in LV diastolic stiffness.

Cardiomyopathy, Hypertrophic↗
PubMed1982

[Weight reduction and blood pressure].

112 patients (78 hypertensives and 34 normotensives) received guidance from a specially trained dietitian on a low-calorie diet. During a mean control period of 10.8 months with a comparable number of visits in each group, the following results were observed: 51% (n = 40) of hypertensive patients achieved a significant weight reduction. In 28% (n = 22) antihypertensive medication was constant and in 23% (n = 18) this medication was reduced or withdrawn. 37% (n = 29) showed no significant changes in body weight or blood pressure and 12% (n = 9) dropped out. In 22 patients a weight reduction of 8.5 kg with a significant fall in blood pressure from 156/99 to 137/90 mm Hg was observed. In 18 hypertensives a weight reduction of 8.5 kg allowed reduction or withdrawal of antihypertensive medication with blood pressure remaining unchanged (139/91 vs. 135/90 mm Hg). Similar results were achieved in 34 normotensive obese patients: 59% (n = 20) had significant weight reduction, 32% (n = 11) no significant reduction in weight or blood pressure, and 9% (n = 3) dropped out. 20 patients with a reduction of 9 kg showed a significant fall in blood pressure from 132/84 to 123/80 mm Hg. The results demonstrate the favourable effect of weight reduction on blood pressure. The time-consuming nature of the frequent and intensive checks should, however, be borne in mind.

Adult↗
PubMed1982

[Occurrence and clinical relevance of thrombocytosis].

Automated routine platelet counting in 18,602 patients revealed thrombocytosis (platelet count above 400,000/mm3) in 9% (n = 1602) of cases. In 32% of the patients with thrombocytosis an acute or chronic inflammatory process was found, 9% had a malignant tumor and 9% anemia. 6% were alcoholics and 6% had a myeloproliferative syndrome. Chronic gastrointestinal disease was found in 4% and postoperative thrombocytosis in 3% of cases. 32% of the thrombocytosis cases could not be classified under any of the known causes of this disorder. In 51% of the cases the platelet count ranged from 400,000 to 450,000/mm3. Primary thrombocythemia often produced clinical symptoms, whereas secondary thrombocytosis almost always was asymptomatic.

Adolescent↗
PubMed1982

[The value of serum ferritin, serum iron and iron-binding capacity in the differential diagnosis of microcytic hypochromic anemia].

Ferritin, iron, total iron binding capacity and transferrin saturation were measured in the serum of 247 patients with microcytic hypochromic anemia. Differentiation into various categories of microcytic hypochromic anemia was based on clinical criteria and on the response to iron treatment. This produced 147 patients with iron deficiency anemia, 35 patients with anemia secondary to infection, 27 patients with anemia due to tumor and 38 patients with thalassemia. Analysis of the iron parameters revealed the reliability of both serum ferritin and transferrin saturation in distinguishing between the various forms of anemia. However, measurement of serum ferritin is slightly more reliable and much less expensive than determination of transferrin saturation.

Anemia, Hypochromic↗
PubMed1982

[Blood pressure, renin angiotensin aldosterone system and other cardiovascular risk factors in children of essential hypertensives (author's transl)].

In the present study, blood pressure, the renin angiotensin aldosterone system, and other cardiovascular risk factors, such as glucose, cholesterine, and triglycerides, were investigated in 294 offspring of essential hypertensives (5-34 years) and in 122 children of normotensive parents (5-34 years). Offspring of essential hypertensives showed statistically significant higher systolic and diastolic blood pressure values than those of normotensive parents (p less than 0.003, less than 0.005, respectively). Furthermore, in children of hypertensive parents a statistically significant higher body weight and body mass index than in controls could be observed (p less than 0.006, less than 0.001, respectively). With the exception of statistically significant, lower mean supine plasma aldosterone values (p less than 0.02) in children of hypertensive parents, no major differences between the two groups were seen in stimulated aldosterone, supine and stimulated plasma renin activity, and plasma cortisol. Furthermore, in the present study, 41 hypertensive parents, 65 (normotensive) spouses of hypertensives, and 47 (normotensive) parents of control children were investigated. As expected, hypertensive parents showed statistically significant higher blood pressure values than parents of control children and their spouses (p less than 0.001). Interestingly, hypertensive parents had not only a higher body mass index than control parents but also than their spouses (p less than 0.01 and less than 0.02, respectively). These findings support a genetic disposition as being the underlying cause of higher body weight in hypertensives and make it less probable that a higher food intake in hypertensive families is responsible for this phenomenon. The results of the present study indicate that early body weight control in children of hypertensive parents may be an important contribution to the prevention of hypertension.

Adolescent↗