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Biomedical subjects

E Teiger

Publications and source records attributed to E Teiger.

At least 37 records · Page 2Linked to original sources
PubMed1999

Coronary microcirculation and cardiovascular pathology.

The recent arrival of new techniques for exploring the coronary microcirculation has facilitated assessment of both the incidence and consequences of disorders of this network in a large number of cardiovascular diseases. The microcirculation is affected in numerous cardiomyopathies in the presence of different cardiovascular risk factors and also following cardiac transplantation. Dysfunction of the microcirculation may correspond to a reduction in the surface of the maximum section of coronary arterioles, which involves multiple mechanisms, although this phenomenon does not appear to play a role in ischaemic heart disease. Reduced coronary flow is most frequently related to vascular rarefaction of multifactorial origin, including greater or lesser degrees of intimal proliferation, perivascular fibrosis, hypertrophy of the media and extrinsic compression.

Cardiovascular Diseases↗
PubMed1999

Coronary microcirculation and cardiovascular pathology.

The recent arrival of new techniques for exploring the coronary microcirculation has facilitated assessment of both the incidence and consequences of disorders of this network in a large number of cardiovascular diseases. The microcirculation is affected in numerous cardiomyopathies in the presence of different cardiovascular risk factors and also following cardiac transplantation. Dysfunction of the microcirculation may correspond to a reduction in the surface of the maximum section of coronary arterioles, which involves multiple mechanisms, although this phenomenon does not appear to play a role in ischaemic heart disease. Reduced coronary flow is most frequently related to vascular rarefaction of multifactorial origin, including greater or lesser degrees of intimal proliferation, perivascular fibrosis, hypertrophy of the media and extrinsic compression.

Cardiovascular Diseases↗
PubMed1999

[Percutaneous suture of femoral artery after diagnostic coronary angiography].

UNLABELLED: Complete local haemostasis after femoral artery catheterization can be performed using percutaneous suture devices. To evaluate efficacy and safety of these systems after diagnostic coronary angiography, we performed a randomized study where patients were treated either with a manual compression (group C) or a percutaneous suture (group T). Fifty patients were included in each group. Patients in group C had to rest at bed during 24 hours while patients in group T had to stand up and walk immediately after complete haemostasis was obtained. All angiographies were performed using a 6 F sheath. All patients had a clinical evaluation and an echography 24 hours after the procedure and all were reached by phone call at 15 days. Both groups were similar in term of age, sex ratio, diabetes, height and weight. Complete haemostasis was obtained in 20 +/- 6 mn in group C and in 6 +/- 10 mn in group T (p < 0.001). Device technical success rate in group T was 90%; 70% of patients walked immediately down the X ray table and 90% before the 4 hours. Ambulation delay was 24 +/- 5 hours in group C and 5 +/- 9 hours in group T (p < 0.0001). Clinical and echographic complications rate were similar in both groups (8%). There was no post procedure complication in group T (especially after ambulation) nor at the phone call. CONCLUSION: Femoral artery percutaneous suture after diagnostic coronary angiography is as safe and working than manual compression. It allows an immediate mobilization and ambulation, far earlier than compression.

Aged↗
PubMed1999

[Physiology of coronary circulation and angioplasty: utopia or clinical reality?].

Small pressure transducer and Doppler quartz placed at the tip of angioplasty guide wire give the opportunity to measure coronary flow physiology parameters, the physiopathologic impact of an epicardic coronary stenosis and the efficacy of its treatment. This gives the opportunity to over ride the coronary imaging limitations. Doppler and pressure investigate a different and complementary aspect of the pressure-flow relation and may be used together in some special cases. Myocardial fractional flow reserve (FFRmyo) and relative coronary reserve concepts allow to evaluate patients with heterogeneous coronary reserve. Clinical application field is very broad and can be applied to each step of coronary angioplasty from the evaluation of intermediate lesions and the indication of angioplasty to the guidance of the procedure to the evaluation of the result, through the stenting indication and the stent placement optimization. Numerous studies has emphasized the role of physiologic coronary assessment in the cathlab. The time and economic gain of such an attitude has to be confirmed by future trials but it is clear now that it is not possible to continue to take decision on the sol visual aspect of a lesion.

Angioplasty, Balloon, Coronary↗
PubMed1999

[Diagnostic value of endocoronary echography].

Intracoronary ultrasound allows in vivo examination of the various layers of the wall of arteries affected by atherosclerosis. Its use in the catheterisation laboratory has therefore allowed better understanding of the mechanism of the action of the various angioplasty procedures, allowing better guidance of the indications and better control of these techniques. It also helps to guide these procedures, thereby facilitating an optimal immediate result, which determines the long-term outcome. The characteristics of intracoronary ultrasound (high resolution, proximity of the arterial wall, echogenicity of constituents of the plaque) make it the instrument of choice to study the composition and structure of the plaque, which determine the clinical presentation and active potential, especially the risk of complications (rupture). The development of image and crude acoustic signal processing techniques have improved the performance of the analysis of these documents and raise hopes of one day being able to predict and anticipate plaque rupture.

Angioplasty↗
PubMed1998

Sequence dependency of the internalization and distribution of phosphorothioate oligonucleotides in vascular smooth muscle cells.

Antisense studies imply the utilization of oligonucleotides (ODN) for sequence-specific down-regulation of genes. This usually consists in assessing antisense sequences versus control sequences (mismatched, inverted, scrambled, randomized or any sequence unrelated to the relevant target). Even though the investigated biological effect (knockdown of an unwanted protein) is observed only with the antisense sequence and weakly, if at all, with any of the control sequences, this is a necessary but not a sufficient condition to demonstrate an antisense effect. Indeed, biochemical parameters such as stability, uptake and subcellular compartmentalization of ODN in a given cellular system are most often sequence-dependent processes. In this work, a series of phosphorothioate ODN of different lengths and sequences were evaluated as to their binding, internalization and subcellular distribution properties in vascular smooth muscle cells. In addition to membrane binding and nuclear accumulation, the partition of ODN in the cytosol of cells was measured by a method based upon controlled permeabilization of the plasma membrane, permitting the recovery of the cytosolic content with minimal damage to the membranes of the endocytic vesicles and lysosomes. We found that the tested ODN showed striking differences in their uptake and distribution in smooth muscle cells. Our results gave rise to the problem of validating the observed biological effects when different sequences of ODN were compared. Cellular studies such as the one presented in this work could help in choosing the proper control sequences among ODN exhibiting similar cell interactions as compared to the antisense sequences. Moreover, this method could be useful for the selection of antisense sequences that can be efficiently internalized and preferentially distributed in the appropriate compartments in cells for in vitro antisense studies.

Animals↗
PubMed1998

Effects of the 14F hemopump on coronary hemodynamics in patients undergoing high-risk coronary angioplasty.

BACKGROUND: The influence of the 14F Hemopump on coronary hemodynamics in patients with coronary artery disease remains unknown. METHODS: Systemic and coronary hemodynamic measurements were obtained in eight patients among 13 who underwent high-risk coronary angioplasty in our institution with the support of the Hemopump. Coronary blood flow velocity was measured with a 0.014-inch Doppler-tipped guide wire both proximal and distal to the target lesion. RESULTS: Angioplasty decreases the diameter coronary stenosis from 76% +/- 21% to 22% +/- 11%. Hemopump support did not change systemic hemodynamics either before or after angioplasty. During angioplasty Hemopump support decreased the pulmonary capillary wedge pressure from 23.5 +/- 8.5 mm Hg to 18.6 +/- 7 mm Hg (p = 0.013). No changes in either heart rate, mean and systolic aortic pressures, and cardiac index were observed throughout the procedure. After successful angioplasty was performed, the ratio of proximal to distal flow velocity decreased from 2.11 +/- 1 to 1.65 +/- 0.2 (p = 0.05). However, Hemopump did not affect absolute coronary blood flow velocities or the phasic pattern of flow velocities (diastolic systolic velocity ratio, diastolic and systolic velocity integrals) either in proximal or distal locations either before or after angioplasty. CONCLUSIONS: This study shows that although the 14F Hemopump produces unloading of the left ventricle, it does not importantly alter coronary hemodynamics when systemic hemodynamics are stable. Whether the Hemopump would maintain or improve coronary blood flow in compromised patients remains to be determined.

Aged↗
PubMed1998

Heart and lung VEGF mRNA expression in rats with monocrotaline- or hypoxia-induced pulmonary hypertension.

Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen that is upregulated during exposure to hypoxia. In this study, we analyzed heart and lung VEGF mRNA expression and examined pulmonary vascular remodeling as well as myocardial capillary density in two rat models of pulmonary hypertension involving exposure to chronic hypoxia (CH) and treatment with monocrotaline (MCT), respectively. The rats were studied after 0.5, 1, 3, 15, and 30 days of exposure to 10% O2 or 1, 6, and 30 days after a subcutaneous MCT injection (60 mg/kg). Both CH and MCT induced pulmonary hypertension and hypertrophy of the right ventricle (RV) with increased RV weight and atrial natriuretic peptide mRNA expression. VEGF mRNA expression as assessed by Northern blot analysis was potently induced after 12 h of hypoxia in both the right and left ventricles. After prolonged exposure to hypoxia, VEGF mRNA returned to baseline in the left ventricle (LV) but remained increased in the RV, where it peaked after 30 days. In MCT rats, VEGF mRNA was unchanged in the LV but decreased by 50% in the RV and by 90% in the lungs after 30 days. VEGF mRNA remained unchanged in the lungs from CH rats. Pulmonary vascular remodeling was more pronounced in MCT than in CH rats. The number of capillaries per RV myocyte was increased in rats exposed to 30 days of hypoxia, whereas it remained unchanged in MCT rats despite a similar degree of RV hypertrophy. Our results suggest that the sustained increase in VEGF expression in the hypertrophied RV during CH may account for the increased number of capillaries per myocyte. In contrast, reduced VEGF expression in the lungs and RV of MCT rats may aggravate pulmonary vascular remodeling and compromise RV myocardial perfusion.

Animals↗
PubMed1998

Polycythemia impairs vasodilator response to acetylcholine in patients with chronic hypoxemic lung disease.

To investigate whether polycythemia associated with chronic hypoxemic lung disease (CHLD) increases vascular resistance by altering endothelium-derived nitric oxide (NO), we examined the responses to acetylcholine (ACh) infusions (5, 10, and 15 mg/min) on hemodynamics and gas exchange in 21 patients with CHLD of varying severity. Patients were classified into two groups based on whether their hemoglobin (Hb) level was less or greater than 15.5 g/dl. In the normocythemic patients (Hb = 13.6 +/- 0.3 g/100 ml, n = 10), ACh decreased pulmonary artery pressure (Ppa) from 30 +/- 2 mm Hg 26 +/- 2 mm Hg (p < 0.01); pulmonary vascular resistance (PVR), from 5.1 +/- 0.4 U/m2 to 3.4 +/- 0.3 U/m2 (p < 0.001); systemic arterial pressure (Psa), from 111 +/- 4 mm Hg to 108 +/- 4 mm Hg (p < 0.05); and systemic vascular resistance (SVR), from 27 +/- 2 U/m2 to 22 +/- 2 U/m2 (p < 0.01); and also increased the cardiac index (CI), from 3.8 +/- 0.2 to 4.7 +/- 0.3 L/min/m2 (p < 0.001). PaO2 fell from 59 +/- 3 mm Hg to 48 +/- 3 mm Hg (p < 0.001) whereas venous admixture (Qs/Qt) rose from 32 +/- 4% to 44 +/- 4% (p < 0.01). In contrast, in patients with polycythemia (17.7 +/- 0.5 g/100 ml, n = 11) ACh failed to produce any changes in PaO2 (49 +/- 2 mm Hg versus 51 +/- 2 mm Hg, p = NS), Ppa (34 +/- 1 mm Hg versus 33 +/- 1 mm Hg, p = NS), PVR (6.7 +/- 0.9 U/m2 versus 6.9 +/- 0.8 U/m2, p = NS) or Psa, but slightly increased the CI, from 3.6 +/- 0.3 L/min/m2 to 3.9 +/- 0.3 L/min/m2 (p < 0.01), and Qs/Qt, from 40 +/- 4% to 45 +/- 3% (p < 0.05). In the 21 patients, negative correlations with Hb concentrations were found for ACh-induced changes in PVR (r = -0.57, p < 0.01), Ppa (r = -0.46, p < 0.01), CI (r = -0.5, p < 0.05), PaO2 (r = -0.79, p < 0.01), and Qs/Qt (r = -0.79, p < 0.01). In the six polycythemic patients who received isovolemic hemodilution, with a decrease in Hb concentration from 18.6 +/- 0.9 g/dl to 15.3 +/- 0.3 g/dl as a result, infusion of ACh, which was without effect before hemodilution, caused decreases in Ppa from 28 +/- 1 mm Hg to 23 +/- 1 mm Hg (p < 0.05) and in PVR from 5.7 +/- 0.8 U/m2 to 3.6 +/- 0.5 U/m2 (p < 0.02), as well as an increase in CI from 3.4 +/- 0.4 L/min/ m2 to 4.1 +/- 0.4 L/min/m2 (p < 0.05). In contrast to ACh, inhaled NO (40 ppm) induced pulmonary vasodilation in both the normocythemic and polycythemic groups. Our results show that high hematocrit (Hct) levels inhibit endothelium-dependent vasodilation in response to ACh in patients with CHLD, possibly through inactivation of endothelial-derived NO by Hb.

Acetylcholine↗
PubMed1997

Alteration of left ventricular diastolic function during coronary angioplasty-induced ischemia: a color M-mode Doppler study.

OBJECTIVES: The aim of this study was to assess the effects of ischemia on diastolic function by analyzing flow propagation velocity with color M-mode Doppler echocardigraphy. BACKGROUND: Color M-mode Doppler echocardiography has been proposed as a method of assessing left ventricular filling. METHODS: Color M-mode Doppler echocardiography and measurement of hemodynamic data were performed simultaneously at baseline and during angioplasty-induced ischemia. Tau was compared with flow propagation velocity. Late diastolic indexes, left ventricular pressure and flow cessation time were also investigated. RESULTS: During ischemia, left ventricular relaxation rate (tau) increased, whereas flow propagation velocity decreased, from (mean +/- SD) 46.8 +/- 10 ms to 72.6 +/- 18.3 ms and from 59.8 +/- 15.8 cm/s to 30 +/- 8 cm/s, respectively (all p < 0.0001). The maximal slowing of flow propagation velocity was observed 20 to 30 s after the beginning of the inflation, coexisting with a notch on the ascending limb of the negative rate of rise of the left ventricular pressure (dP/dt) curve. Flow propagation velocity was correlated with tau both at baseline (r = 0.53, p < 0.05) and during inflation (r = 0.53, p < 0.03). Left ventricular end-diastolic pressure increased during ischemia from 13.5 +/- 8 mm Hg at baseline to 27.5 +/- 7 mm Hg, while a premature cessation of the entering flow occurred -13.8 +/- 23 ms before the next Q wave onset, compared with 4.5 +/- 19.6 ms after the Q wave onset at baseline (all p < 0.0001). CONCLUSIONS: The analysis of flow propagation velocity showed that early filling is highly dependent on left ventricular relaxation rate, particularly through the phenomenon of asynchrony. During ischemia, the premature cessation of late filling is associated with increased diastolic pressures.

Angioplasty, Balloon, Coronary↗
PubMed1997

Role of coronary artery lumen enlargement in improving coronary blood flow after balloon angioplasty and stenting: a combined intravascular ultrasound Doppler flow and imaging study.

OBJECTIVES: This study sought to examine the mechanism of increasing coronary flow reserve after balloon angioplasty and stenting. BACKGROUND: Coronary vasodilatory reserve (CVR) does not improve after percutaneous transluminal coronary angioplasty in > or = 50% of patients, postulated to be due to impaired microvascular circulation or inadequate lumen expansion despite adequate angiographic results. METHODS: To demonstrate the role of coronary lumen expansion, serial coronary flow velocity (0.014-in. Doppler guide wire) was measured in 42 patients before and after balloon angioplasty and again after stent placement. A subset (n = 17) also underwent intravascular ultrasound (IVUS) imaging of the target sites after angioplasty and stenting. CVR (velocity) was computed as the ratio of adenosine-induced maximal hyperemic to basal average peak velocity. RESULTS: The percent diameter stenosis decreased from (mean +/- SD) 84 +/- 13% to 37 +/- 18% after angioplasty and to 8 +/- 8% after stenting (both p < 0.05). CVR was minimally changed from 1.70 +/- 0.79 at baseline to 1.89 +/- 0.56 (p = NS) after angioplasty but increased to 2.49 +/- 0.68 after stent placement (p < 0.01 vs. before and after angioplasty). IVUS lumen cross-sectional area was significantly larger after stenting than after angioplasty (8.39 +/- 2.09 vs. 5.10 +/- 2.03 mm2, p < 0.05). Anatomic variables were related to increasing coronary flow velocity reserve (CVR vs. IVUS lumen area: r = 0.47, p < 0.005; CVR vs. quantitative coronary angiographic percent area stenosis: r = 0.58, p < 0.0001). CONCLUSIONS: In most cases, increases in CVR were associated with increases in coronary lumen cross-sectional area. These data suggest that impaired CVR after angioplasty is often related to the degree of residual narrowing, which at times may not be appreciated by angiography. A physiologically complemented approach to balloon angioplasty may improve procedural outcome.

Angioplasty, Balloon, Coronary↗
PubMed1997

Induction of nitric oxide synthase activity in pulmonary arteries from normoxic and chronically hypoxic rats.

Chronic hypoxia has recently been shown to upregulate inducible nitric oxide synthase (iNOS) gene expression in rat lung. In the present study, we questioned whether induction of NO synthesis could alter the reactivity of pulmonary arteries (PA) from chronically hypoxic (CH) rats. Dose-response curves to phenylephrine (PE) 10(-9) to 5 x 10(-6) M) were examined in PA rings as well as response to L-arginine analogues in isolated lungs from CH or normoxic (N) rats after various incubation times. Although maximal contraction to PE did not differ in PA from CH rats compared to N rats at time 0 (361 +/- 53 vs 506 +/- 52 mg, respectively), it was markedly decreased after prolonged incubation (149 +/- 28 vs 386 +/- 47 mg, respectively, at 4 h; p < 0.001). This phenomenon persisted after endothelial-denudation, but was reversed by NG-monomethyl-L-arginine (L-NMMA) (5 x 10(-4) M) and prevented by actinomycin D (2 x 10(-6) M). In contrast, maximal contraction to PE in aorta from CH rats was similar at time 0 and 4 h. After a short incubation, PA contraction to L-NMMA was greater in CH than in N rats (96 +/- 17 vs 33 +/- 9 mg at 90 min; p < 0.05), was abolished after endothelial denudation, but persisted in CH rats in the presence of calmidazolium (5 x 10(-4) M). At 4 h, contraction to L-NMMA was abolished in endothelium-denuded PA from N rats but only attenuated in those from CH rats. In salt solution perfused lungs, L-NMMA added 30 or 90 min after isolation did not alter baseline pressure in N rats but caused its increase in CH rats. Whereas iNOS messenger ribonucleic acid (mRNA) was detectable by reverse-transcriptase polymerase chain reaction in the PA wall of N or CH rats after 4 h of incubation, it was absent in both at the time of isolation. In contrast, there was evidence of iNOS mRNA in lungs from CH rats at the time of isolation but no signal in those from N rats. In conclusion, there is induction of nitric oxide synthase activity in pulmonary arteries from normoxic and chronically hypoxic rats after prolonged incubation, but this effect is more pronounced in pulmonary arteries from chronically hypoxic rats.

Animals↗
PubMed1996

Sympathetic stimulation overrides flow-mediated endothelium-dependent epicardial coronary vasodilation in transplant patients.

BACKGROUND: Abnormal coronary vasomotor responses have been described in transplant patients. The aim of this study was to evaluate the graft epicardial vasomotor responses to different stimuli that increase coronary blood flow. METHODS AND RESULTS: Twelve heart transplant recipients with angiographically normal epicardial coronary arteries were compared 2.7 +/- 1.2 months after surgery with 6 control subjects. Coronary flow velocity was measured with a guidewire Doppler. Coronary diameter changes of the proximal and midportion of the left anterior descending coronary artery were assessed by quantitative coronary angiography during rapid atrial pacing, cold pressor test, supine exercise, and subselective infusion of papaverine and after intracoronary injection of linsidomine (SIN-1). Catecholamine plasmatic levels were determined at the different stages of the protocol. In 6 other transplant patients, a cold pressor test was performed before and after intracoronary infusion of phentolamine (10 micrograms.kg-1.min-1). Coronary flow velocity increased significantly in both groups during each phase of the protocol. In control subjects, dilation was observed in response to atrial pacing (8.7 +/- 7.6%; P < .05), CPT (8.8 +/- 2.3%; P < .01), exercise (14.5 +/- 9.4%; P < .001), and papaverine infusion (14.2 +/- 6.1%; P < .001) and after injection of SIN-1 (26.8 +/- 11.9%; P < .001). In transplant patients, similar dilation was observed during atrial pacing (8.2 +/- 8.3%; P < .05) and papaverine infusion (14.6 +/- 7.8%; P < .001) and after SIN-1 (25.8 +/- 10.8%; P < .001). CPT and exercise caused slight constriction (-3.5 +/- 4.5% and -2.7 +/- 10.5%, respectively; both P < .001 versus control subjects). Norepinephrine plasmatic levels increased in both groups during CPT and exercise. Slight constriction during the cold pressor test (-4.5 +/- 9.6%) changed to dilation (6.8 +/- 7.0%) after alpha-blockade with phentolamine (P < .001). CONCLUSIONS: These results show that flow-mediated, endothelium-dependent vasodilation is preserved early after trans-plantation. Sympathetic stimulation, which overrides the endothelium-dependent mechanism, can be related to hypersensitivity to catecholamines due to denervation.

Adrenergic alpha-Antagonists↗
PubMed1996

Apoptosis in pressure overload-induced heart hypertrophy in the rat.

Pressure overload induces cardiac growth in the rat, which implies the hypertrophy of cardiac muscle cells and proliferation of nonmuscle cells. The cardiac cell loss observed in parallel has generally been attributed to necrosis. Using an in situ assay, we demonstrated a phase of apoptosis or programmed cell death during the first 7 d after pressure overload with a peak at day 4 while cardiac growth continued for over 30 d. The increase in apoptosis was confirmed by quantification of 180-1500-bp DNA oligonucleosomes with agarose gel electrophoresis and in situ labeling via 3'-terminal deoxynucleotidyl transferase assay. While some apoptosis was observed in the basal state in nonmuscle cells, pressure overload induced apoptosis mainly in cardiomyocytes. These data suggest that cardiac hypertrophy is initiated by a wave of apoptosis of cardiomyocytes. Thus, apoptosis may be involved in the pathogenesis of heart remodeling.

Adaptation, Physiological↗
PubMed1996

Effect of delayed percutaneous transluminal coronary angioplasty of occluded coronary arteries after acute myocardial infarction.

Whether angioplasty of occluded vessels after myocardial infarction may have beneficial effects on left ventricular function remains unknown. Patients with a first myocardial infarction and thrombolytic therapy who had an occluded infarct-related vessel at delayed coronary angiography were referred systematically for an elective coronary angioplasty performed between 3 and 4 weeks after the myocardial infarction. All patients underwent stress-redistribution-reinjection thallium-201 single-photon emission computed tomography for myocardial viability assessment. Prior angioplasty, a quantitative evaluation of global and regional left ventricular function, was performed. The study group consisted of 38 patients (aged 57 +/- 10 years); 18 had anterior wall infarctions and 20 inferior wall infarctions, but before angioplasty 3 had a patent artery and were excluded. Angioplasty was successful in 30 patients. At follow-up 13 patients (43%) had an occluded coronary artery. In contrast with patients with an occluded coronary artery at follow-up, those with a patent coronary artery had no left ventricular enlargement and had an improvement in both left ventricular ejection fraction (from 48 +/- 9% to 52 +/- 9.8%, p = 0.002) and regional wall motion index (delta = +0.95 SD, p <0.01). In patients with a patent vessel at follow-up, there was a positive correlation between the number of myocardial viable segments and improvement of the infarct zone wall motion (r = 0.52; p = 0.035), and the number of necrotic segments at baseline was positively correlated to the 4-month changes in end-diastolic volume indexes (r = 0.6; p = 0.04). Thus, elective revascularization of occluded coronary arteries with viable myocardium after myocardial infarction improves left ventricular function and lessens remodeling if the artery remains patent during follow-up.

Aged↗
PubMed1996

Apoptosis and vascular wall remodeling in hypertension.

Vascular structure plays a key role in the pathogenesis of hypertension. Because it is less readily reversible than protein accumulation, DNA accumulation in the arterial wall may be considered as a record of past episodes of vascular growth, contributing to the persistence of the vascular disease. Apoptosis, a ubiquitous and highly regulated form of programmed cell death that is involved in tissue morphogenesis and homeostasis as the essential counterpart of cell replication, is potentially involved in the regulation of vascular structure, via the deletion of cells in the vessel wall. We discuss how the current knowledge on apoptosis may provide insights into the pathogenesis of vascular wall remodeling, with an emphasis on the biology of vascular smooth muscle cells. Evidence suggests that heightened cell replication rates are often associated with increased apoptosis, as for smooth muscle cells in genetic hypertension or in arterial repair after injury. However, apoptotic cell death may also be regulated independently of cell growth. The triggering of apoptosis depends on a balance of environmental cues that are not specific to apoptosis. However, there is a common set of key biochemical events mediating apoptosis (i.e., committing the cell to die), thus providing a basis for the design of novel pharmacological strategies specifically targeting apoptotic cell death. The identification of biochemical markers of apoptosis and other methodological advances will ultimately help in understanding the role of apoptotic cell death in vascular remodeling and hypertensive end-organ damage.

Animals↗