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J J Schipperheyn

Publications and source records attributed to J J Schipperheyn.

At least 19 recordsLinked to original sources
PubMed1998

[Incidental high blood pressure in family practice: due to hypertension and/or left ventricular hypertrophy in more than half of the patients].

OBJECTIVE: To determine if patients with incidentally high blood pressure actually have hypertension and if these patients have an increased left ventricular mass. DESIGN: Cross-sectional study. SETTING: Two family practices with 8 general practitioners in Leiden and Noordwijk, the Netherlands. METHODS: From the Family Practice Network in the Leiden area 133 (67%) out of 200 patients with incidental high blood pressure, who did not receive antihypertensive medication, participated in the study. Their blood pressure was measured 6 times with a mercury manometer, an automatic, non-invasive ambulatory blood pressure monitoring during 24 hours was performed once and their left ventricular mass was measured by means of echocardiography. RESULTS: Of the 133 selected patients 46% had a mean diastolic blood pressure > 95 mmHg measured with the mercury manometer and 64% had a mean 24-hr diastolic blood pressure > 90 mmHg measured with the ambulatory blood pressure monitor. The correlation between both blood pressure measurements was moderate (correlation coefficient 0.73). Left ventricular hypertrophy was found in 53% of the patients, irrespective of their blood pressures. CONCLUSION: In this investigation 45-65% of patients with an incidentally high blood pressure had a mean diastolic pressure > 95 mmHg as measured with a mercury manometer and (or) a mean 24-hr diastolic blood pressure > 90 mmHg as measured with the ambulatory blood pressure monitor; 53% had left ventricular hypertrophy.

Adolescent↗
PubMed1997

Beneficial effect of enalapril on left ventricular remodelling in patients with a severe residual stenosis after acute anterior wall infarction.

OBJECTIVE: The present study was designed to evaluate the effects of early angiotensin converting enzyme (ACE) inhibition on left ventricular enlargement in patients with anterior wall infarction following reperfusion therapy. METHODS: Seventy-one consecutive patients with an anterior wall myocardial infarction were randomly allocated to enalapril (n = 36) or placebo (n = 35). All patients received either thrombolytic therapy (n = 46) or underwent primary coronary angioplasty (n = 25). Medication was started within 48 h admission to hospital and continued for 48 weeks. The process of left ventricular remodelling was assessed with two-dimensional echocardiography at 3 weeks and 1 year after the acute onset, and was related to the severity of the residual stenosis of the infarct-related artery. RESULTS: Baseline left ventricular ejection fraction was 39.2% +/- 8.7%. During the study period left ventricular end-diastolic volume index increased from 48.2 +/- 9.9 ml.m-2 to 54.6 +/- 12.2 ml.m-2 at 3 weeks, and to 59.4 +/- 17.0 ml.m-2 after 1 year I control patients (P < 0.001). In the enalapril-treated patients, left ventricular end-diastolic volume index increased from 50.0 +/- 16.1 to 57.7 +/- 19.3 ml.m-2 at 3 weeks, and to 61.9 +/- 22.7 ml.m-2 after 1 year (P < 0.001). Both at 3 weeks and after 1 year, no overall differences in left ventricular volumes were observed between the enalapril and the placebo group (both ns). However, patients with a residual stenosis severity of > or = 70% in the infarct-related artery (n = 43) showed significant attenuation of remodelling by enalapril (n = 22) when compared to placebo (n = 21). In patients on enalapril, left ventricular end-diastolic volume index increased from 47.0 +/- 13.0 to 53.7 +/- 17.7 ml.m-2 compared to 48.0 +/- 9.6 to 60.3 +/- 16.3 ml.m-2 in control patients (P < 0.03). Also diastolic filling parameters were significantly improved in patients with > or = 70% residual stenosis. CONCLUSION: In patients with an anterior wall infarction and a severe residual infarct-related coronary artery stenosis following reperfusion, treatment with enalapril prevents the process of left ventricular remodelling. As left ventricular dilatation is an early process we suggest that treatment with ACE inhibition should be started as soon as possible in this group of patients.

Aged↗
PubMed1996

Reproducibility of left ventricular size, shape and mass with echocardiography, magnetic resonance imaging and radionuclide angiography in patients with anterior wall infarction. A plea for core laboratories.

After myocardial infarction, left ventricular volume and ejection fraction can be assessed by echocardiography, magnetic resonance imaging and radionuclide angiography to guide therapy and determine prognosis. Whether a measured parameter gives the same results irrespective of the method used and the observer who performs the analysis is only partly known. Intra-observer and inter-observer variability were determined for echo and magnetic resonance imaging. Left ventricular ejection fraction measured by these techniques was related to radionuclide angiograms performed in the same period. Intra-observer variability for both echo and MRI was low and in most instances below 5%. Inter-observer variability for the echo and MRI measurements were substantially higher than intra-observer variability. Comparison of the three imaging modalities revealed systematic differences. Therefore, in clinical studies, left ventricular volume and function parameters have to be measured with the same technique and by the same observer in qualified core laboratories.

Adult↗
PubMed1996

Regional myocardial shape alterations in patients with anterior myocardial infarction.

OBJECTIVE: To assess the impact of regional left ventricular curvature in patients with an acute anterior myocardial infarction on ventricular volume. METHODS: Left ventricular curvature was calculated at 100 points from apical four chamber echocardiograms of 68 patients with an acute anterior wall infarction. Curvature at any point of the contour was defined as the reciprocal of the radius of the circle that intersects that point tangentially and was independent of volume and geometric assumptions. Curvature, volume and shape of the patient group was compared with these measurements in 20 normal volunteers. RESULTS: Diastolic curvature differed at the borderzone of the infarct and the apical area. In the basal septal area (point 9-18) mean curvature was lower in the patient group (0.1 +/- 2.7 versus 2.1 +/- 0.7; p < 0.0001) as compared to the normal individuals. In the mid-septal area (point 22 to 27), mean curvature was more concave (-0.1 +/- 2.6) in the patient group corresponding to in the normal population (-0.4 +/- 1.3) p < 0.005. In the apex point 52 and 53 diverged with a curvature of 9.9 +/- 1.9 in patients versus 9.4 +/- 2.9 p < 0.005 in normal individuals. Systolic curvature diverged at the basal septum (point 1-4) with a mean curvature of 1.4 +/- 1.1 in patients compared to 3.5 +/- 2.5 in normal individuals p < 0.01. Curvature differed also in the mid-septal region (point 9-29) with a curvature of -1.7 +/- 1.2 in patients versus 0.4 +/- 0.9 (p < 0.01) in normal individuals and in the apical septum (point 48-52) with a curvature of 16.6 +/- 5.2 in patients and 13.9 +/- 2.6 (p < 0.0001) in healthy individuals Separation of patients with the greatest curvature alteration to those with minor curvature change revealed, that baseline curvature analysis can discriminate patients at risk for left ventricular remodelling. CONCLUSION: Regional curvature analysis correctly identifies the geometric changes induced by myocardial infarction. Apical systolic curvature can distinguish those patients that are at risk for left ventricular remodelling from those who are not at risk.

Adult↗
PubMed1995

Combining salicylate and enalapril in patients with coronary artery disease and heart failure.

OBJECTIVE: To study the effects of adding a salicylate to the angiotensin converting enzyme inhibitor enalapril in patients with heart failure due to coronary artery disease. DESIGN: Double blind, crossover study for three days in hospital followed by an extended similar study outside hospital over two months of once daily enalapril plus salicylate and enalapril plus placebo. SETTING: Tertiary referral centre. PATIENTS: 20 patients with heart failure due to myocardial infarction (New York Heart Association class II or III) and an ejection fraction less than 0.40. Twelve patients completed the two parts of the study. MAIN OUTCOME MEASURES: Blood pressure, plasma converting enzyme activity; plasma angiotensin II and noradrenaline concentrations; excretion of metabolites of renal and systemic prostanoids. RESULTS: The unloading effect of first and second dose of enalapril in the morning lasted only during the day; in the extended study it lasted 24 hours because of the drug's accumulation. Converting enzyme inhibitors attenuate the breakdown of bradykinin and therefore enhance prostaglandin E2 synthesis mediated by bradykinin. Evidence was found of such a prostaglandin E2 mediated contribution to ventricular unloading by enalapril, which was blocked by salicylate. The contribution, however, was small and variable, and salicylate addition had on average no significant de-unloading effect during the day. Unloading was abolished in only three of the 20 patients in the short term study and in one of the 12 in the extended study. At night, when other effects of enalapril on blood pressure had waned and the bradykinin induced effect persisted, salicylate significantly reduced the remaining small unloading effect. No effect was seen of salicylate addition on reversal of remodelling. Enalapril reduced angiotensin II induced synthesis of systemic and renal prostaglandin I2 and thromboxane A2, initially only during the day, but later also at night. It thereby masked suppression of thromboxane A2 synthesis by salicylate, which is the effect to which reinfarct prevention by salicylate is attributed. CONCLUSION: The risk is low that salicylate will substantially reduce the benefit of enalapril in patients with heart failure by de-unloading the ventricle. Like other effects induced by bradykinin significant de-unloading occurs in only a minority of the patients. In the presence of enalapril, however, salicylate will probably not be as effective as expected in reducing reinfarction risk, because enalapril already reduces thromboxane A2 synthesis effectively in patients with heart failure and no further reduction by salicylate was found.

Adult↗
PubMed1992

Left ventricular filling after long-term angiotensin converting enzyme inhibition in congestive heart failure.

As a rule, left ventricular relaxation is impaired in patients with coronary artery disease and congestive heart failure. In addition, the passive elastic properties in early and late diastole change when the ventricle dilates. Diastolic properties of the left ventricle were studied in 11 patients with congestive heart failure class II-IV (NYHA) before and 3 months after 10-20 mg enalapril was added to their regimen of salt restriction, a diuretic and occasionally digitalis. Haemodynamic studies were performed using radionuclide angiography and simultaneous pressure-volume measurements. Systemic vascular resistance decreased from 1479 to 1182 dynes.s.-1 cm-5 (P < 0.05) and left ventricular end-diastolic pressure from 19.2 to 15.9 mmHg (P < 0.05). Left ventricular end-diastolic volume index decreased from 130 +/- 22 to 81 +/- 22 ml (P < 0.01). Indices of early diastolic relaxation, such as peak filling rate (1.43 +/- 0.46 to 1.49 +/- 0.84 EDV/s), time to peak filling rate (460 +/- 70 to 490 +/- 70 ms), peak negative dP/dt (-903 +/- 190 to -891 +/- 190 mmHg/s) and tau, the time constant of isovolumic pressure decay (58.7 +/- 14.4 to 48.4 +/- 15.2 ms) did not change significantly. In nine patients pressure-volume loops shifted to the left in all patients but one due to reduction in end-systolic and end-diastolic volume. The steepness of the diastolic part of the pressure-volume relationship increased, indicating an increase in chamber stiffness. The stiffness constant increased about 25% towards a more normal value. The alteration in stiffness seemed to be mainly due to the change of the geometry of the ventricle and not to a major change in the visco-elastic properties of the ventricular wall. In conclusion, regression of remodelling induced by enalapril does not change diastolic function parameters in patients with chronic congestive heart failure beyond the changes caused by regression of ventricular dilation.

Blood Pressure↗
PubMed1991

Influence of angiotensin converting enzyme inhibition on pump function and cardiac contractility in patients with chronic congestive heart failure.

Eleven patients with coronary artery disease and chronic heart failure were studied before and three months after the angiotensin converting enzyme inhibitor enalapril was added to their frusemide medication. The following were measured: left ventricular pressure and volume with transient occlusion of the inferior vena cava, radionuclide angiography, and hormone concentrations in plasma. As in other reported studies, the clinical condition of the patients improved and their exercise tolerance increased moderately. Addition of enalapril reduced end diastolic and systolic pressure, reduced ventricular volume, and concomitantly increased the ejection fraction. The end systolic pressure-volume relation shifted to the left as it did in a similar animal study. In the animal study unloading by a vasodilator did not induce a leftward shift, so it can be inferred that in the present study unloading combined with a decrease in the angiotensin concentration was instrumental in remodelling the heart. Though unloading was expected to have a beneficial effect on the oxygen supply/demand ratio of the heart, the patients still showed the same drop in the ejection fraction during exercise as they did before treatment with enalapril, and early diastolic filling did not improve. Normally, regression of cardiac dilatation is only found if pump function improves; the present study showed that unloading in combination with angiotensin converting enzyme inhibition reshapes the ventricle without improving intrinsic pump function.

Aged↗
PubMed1991

Cardiac remodelling and myocardial contractility in patients with congestive heart failure treated with furosemide and enalapril.

Eleven patients with congestive heart failure class II-IV (NYHA) caused by ischemic heart disease were studied before and three months after adding enalapril to their treatment with furosemide. After an infarction the heart dilates gradually, mainly as a result of slippage of myocardial fiber bundles. It is known that the addition of an ACE-inhibitor to the medical treatment unloads the heart and gradually, within a period of 3 months, reduces heart size. Objectives of this study were to demonstrate remodelling by recording diastolic pressure-volume relations before and after treatment. The study addresses the question of whether regression of dilation, induced by the ACE-inhibitor treatment, improves the oxygen supply-demand ratio and, as a result, the contractility of the heart muscle. Treatment resulted in a reduction of vascular resistance (1479 to 1182 dyn.s.cm-5, p less than 0.05) and of the left ventricular end-diastolic (130 to 108 ml per m2 body surface area, p less than 0.05) and end-systolic (102 to 81 ml per m2 body surface area, p less than 0.01) volume index. The slope of the end-systolic pressure-volume relation, measured using vena cava occlusion and beat-to-beat recording of pressure and volume loops, remained unchanged. Indices of oxygen-supply demand ratio such as a drop of ejection fraction during exercise and parameters of active diastolic relaxation also did not change. Addition of an ACE-inhibitor induces regression of ventricular dilation, but no indications were found that it improves the condition of the cardiac muscle.

Aged↗
PubMed1990

Imaging of acute myocardial infarction in pigs with Indium-111 monoclonal antimyosin scintigraphy and MRI.

Indium-111 antimyosin F(ab')2 was used in a series of scintigraphic studies on experimentally induced myocardial infarctions in pigs. Antimyosin distribution recorded by planar images of in vivo pigs and by single photon emission computed tomography (SPECT) of excised hearts delineated areas of myocardial necrosis if infarct volume exceeded 3.3 cm3. Scintigraphic images were compared with magnetic resonance images (MRI) obtained from excised hearts and with photographs of slices of the hearts. Infarct size and localization determined with antimyosin were compared. The MR images, with or without gadolinium-DTPA (Gd-DTPA), of the in vivo pigs were all false-negative; some myocardial wall thinning and high bloodpool signals were visible. Results show that both the antimyosin and the MR technique are specific methods for the visualization of induced myocardial necrosis in this animal model. However, the use of antimyosin is limited to a period ranging from 24 to 72 hours after infarction.

Animals↗
PubMed1990

Comparison of rigid and flexible rings for annuloplasty of the porcine mitral valve.

Seven rigid (Carpentier) and six flexible (Duran) annuloplasty rings were implanted in healthy pigs. First, in the intact pig, cinefluoroscopy was used to record movements of the anulus. Results were compared with data from three pigs instrumented with a continuous radiopaque marker on the anulus. Pump function of all hearts with annuloplasty rings and function of the mitral valve were studied 4-6 weeks after the operation, first in the exposed heart and then subsequently in the isolated heart in a perfusion chamber at maximal filling pressure and normal or low arterial pressure. Separation of the blood-perfused coronary circulation from the crystalline solution pumped by the left heart allowed videoendoscopy of the working valve. Flexible rings interfered less with normal movements of the mitral anulus than rigid rings and caused less impairment of filling of the basal part of the ventricle, and the unloaded stroke volume was 16% larger. For normal arterial pressures, the differences were smaller and will be difficult to detect in clinical situations. A stiff anulus was seen to be pushed underneath the aortic valve during systole, which caused a mild subvalvular obstruction. The mean diastolic pressure gradient across rigid annuloplasty rings was slightly larger than across flexible rings of the same or slightly smaller diastolic size. Rigid rings change the pattern of movement of the leaflets; the mural leaflet remains immobile throughout diastole. Although Duran rings interfere less with valvular function and filling of the basal part of the ventricle than do Carpentier rings, the differences are small and probably only of limited clinical importance.

Animals↗
PubMed1989

Influence of mitral valve prosthesis or rigid mitral ring on left ventricular pump function. A study on exposed and isolated blood-perfused porcine hearts.

We have studied the effects on cardiac function of a Björk-Shiley mitral prosthesis or a rigid mitral ring implanted in pigs for as long as 6 weeks. We studied these effects first in the exposed heart and subsequently in the isolated heart. The coronary arteries were cannulated and perfused with fresh whole blood. The left ventricle was filled with an electrolyte solution and was allowed to pump against an artificial load. Studies were completed in 37 of 45 animals (19 controls, 12 with mitral prostheses and six with mitral rings). In the open-thorax situation, surgically treated hearts differed little from controls, apart from a higher pressure drop over the mitral ostium. Compared with controls, isolated hearts with a prosthesis showed a 28% lower peak isovolumic pressure and a 25% lower unloaded maximal stroke volume; hearts with a mitral ring showed 14% and 25% lower values, respectively. Prosthetic valve or ring implantation causes obstruction of the mitral ostium, impedes pressure development, and restricts movement of the basal ventricular wall. Resection of the native valve doubles the loss of contractile function.

Animals↗
PubMed1987

Cardiac abnormalities in myotonic dystrophy. Electrocardiographic and echocardiographic findings in 65 patients and 34 of their unaffected relatives. Relation with age and sex and relevance for gene detection.

Sixty-five patients with a definite diagnosis of myotonic dystrophy (MD) and 34 of their presumably unaffected relatives were examined cardiologically, including ECG in all and echocardiography in 61 and 32 persons respectively, in order to investigate the frequency of cardiac abnormalities, their clinical importance and their potential value as a preclinical marker in the diagnosis of MD. Atrioventricular conduction (AVC) abnormalities were found in 18/33 (54%) of affected males and in only 5/32 (16%) of affected females (P = 0.0025). Intraventricular (IVC) conduction abnormalities were encountered with similar frequency in both sexes: in 12/33 (36%) of affected males and 10/32 (31%) of affected females. Mitral valve prolapses (MVP) were seen more often in affected females: 9/31 (29%) of affected males vs 15/30 (50%) of affected females have MVP (P = 0.16). A previously undescribed finding was that of pericardial effusions in 5 affected and in 1 unaffected person. All affected males with MVP also had conduction abnormalities, but cardiac findings were not interrelated otherwise. None of the cardiac abnormalities mentioned were age-related. Only 8/65 (12%) of patients had cardiac symptoms, all of which were the result of conduction defects. As far as can be judged from a transversal study, the value of cardiac examination of this kind as a preclinical test for the diagnosis of MD is modest. It is argued that IVC-abnormalities, but not AVC-disturbances or MVP, in clinically unaffected relatives may indicate that they are preclinical heterozygotes. The significance of pericardial effusion for the diagnosis of MD awaits further evaluation.

Adolescent↗
PubMed1985

Cold ischemic arrest: comparison of calcium-free and calcium-containing solutions.

Isolated pumping rat hearts, perfused with reconstituted blood, were studied to compare the effects of 30 minutes of ischemic arrest following calcium-free or normal, calcium-containing cold cardioplegia on recovery of mechanical function, lactate production, myocardial adenosine triphosphate concentration, and release of creatine kinase (CK). As in clinical situations, the volume of the infusate was only three to four times the intracavitary blood volume. Hearts arrested with calcium-free solution showed incomplete recovery of mechanical function, whereas hearts arrested with calcium-containing solution recovered completely. After calcium-free arrest, stroke volume recovered to 76 +/- 29% (standard deviation [SD]) of its prearrest value. Enzyme release (CK) was significantly higher after calcium-free cardioplegia (7.7 +/- 4.6 units [SD]) than after cardioplegia with normal calcium (2.1 +/- 1.6 units [SD]). Since the addition of only 0.025 mmol calcium ions to a liter of calcium-free solution completely prevented its negative effect, it was concluded that calcium-free cardioplegia may cause limited but pronounced damage to myocardial cells, presumably because it removes calcium from the cellular membranes--the so-called calcium paradox. Probably due to residual calcium in blood and extracellular fluid, the damage is not so extensive after calcium-free cardioplegia as to be noticeable in clinical surgical situations. Residual calcium in the heart does not exclude the possibility, however, that a calcium paradox occurs in small scattered areas of the heart.

Adenosine Triphosphate↗
PubMed1984

The pathophysiology of potassium and magnesium disturbances. A cardiac perspective.

Sodium (Na+) and calcium (Ca++) ions are both involved in the activation of cardiac muscle cells. Na+ ions initially depolarise the cell, and the cell-inward flux of Ca++ ions maintains the plateau phase of the action potential. Ca++ ions trigger the release of more Ca++ ions from the sarcoplasmic reticulum. The free Ca++ ions inside the cell subsequently activate the formation of actomyosin complexes and initiate the contraction. Potassium (K+) and magnesium (Mg++) ions modulate the actions of Na+ and Ca++. Hyperkalaemia lowers the membrane potential, and thereby reduces excitability and conduction velocity. Doubling of the K+ concentration may stop the heart, but slightly increased K+ concentrations may increase the risk of arrhythmia. Hypokalaemia reduces potassium conductance of the muscle cell. Instead of hyperpolarising the cell, as one might expect, the myocardium depolarises in a low-K+ solution. Membrane resistance increases and depolarising currents are insufficiently balanced by K+ conductance changes. In the case of low K+, the cells are unstable and excitability is increased. In addition, hypokalaemia increases the risks of digitalis treatment and enhances the arrhythmogenic effect of digitalis. Although cardiac muscle contains a relatively high concentration of Mg++, the free Mg++ concentration is probably low. Outside the cell, the free Mg++ concentration is about 0.5 to 0.7 mmol/L, and there is probably little or no gradient across the cell membrane. A passive carrier-mediated influx of Mg++ ions balanced by an active countertransport keeps intracellular Mg++ concentrations relatively constant. Membrane permeability is low and Mg++ has little direct effect on the membrane potential.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1983

Transient in oxygen uptake after step-increase of workload under beta-adrenoceptor blockade or vasodilation.

The effect of vasodilation (with nifedipine) or beta-adrenergic receptor blockade (with propranolol, alprenolol or metoprolol) on the rate of rise of oxygen uptake and heart rate were studied in 14 healthy subjects after a step-wise increase of workload from a light to a moderate exercise intensity. Under beta-adrenergic receptor blockade steady state oxygen uptake at both workload levels was equal to control values; heart rate went up to 111 min-1 (s.d.:15) vs 150 min-1 (s.d.:24) for the control experiments. The half-times of the oxygen uptake transient were unchanged. After vasodilation with nifedipine heart rates were higher (20% for the lower and 12% for the higher exercise level) but steady state oxygen uptake levels and rate of rise were also unchanged. It is concluded that the rate of rise of oxygen supply to working skeletal muscles after a stepwise increase of load is not reduced either by a beta-adrenergic receptor blocking drug nor by a vasodilating agent. Discomfort during exercise appears to be a subjective phenomenon related to reduced skin circulation and sweating under beta-adrenergic receptor blockade, or to headache and congestion after vasodilatory drug administration. These side-effects are not caused by a reduced oxygen supply of muscle, neither under steady state situations nor under rapid changing workload conditions.

Adolescent↗