Subcellular distribution of cardiac fatty acid-binding protein in bovine heart muscle and quantitation with an enzyme-linked immunosorbent assay.

Several types of the 14-15 kDa fatty acid-binding proteins (FABPs) are known to occur in the cytosol of mammalian cells. With antibodies raised against the cardiac-type protein from bovine heart, immunoblots indicated a more widespread distribution of the cardiac FABP in subcellular fractions, such as mitochondria and nuclei. A detailed view was obtained when the post-embedding protein A-gold labeling method was applied to cross-sections of heart cells and isolated subcellular fractions. Cardiac FABP in myocytes was associated with myofibrils and localized within mitochondria and nuclei. After subfractionation of mitochondria, the binding protein was recovered with matrix proteins only. A non-competitive enzyme-linked immunosorbent assay (ELISA) of the direct type was developed specifically for bovine cardiac FABP. This assay was sensitive in the range of 0.05 to 1 ng, and concentrations of cardiac FABP per mg protein were found for cytosol, matrix and nuclei to be around 3.18, 0.18 and 0.03 micrograms, respectively. The newly found compartmentation of cardiac FABP in the heart cell must be considered when the true functions of the protein, yet to be defined, are studied.

Reduced acute thrombus formation results in decreased neointimal proliferation after coronary angioplasty.

OBJECTIVES: We tested the hypothesis that reduced acute platelet deposition after angioplasty results in reduced late neointimal proliferation. BACKGROUND: Platelet-mediated mechanisms contribute to smooth muscle cell proliferation and migration. METHODS: Indium-111-labeled platelets were injected 16 h before coronary stent angioplasty in 10 Göttinger minipigs: group 1 (n = 5) = heparin (100-U/kg bolus) before angioplasty; group 2 (n = 5) = recombinant hirudin (CGP 39393, 1.0-mg/kg body weight bolus intravenously), followed by subcutaneous doses of 6 to 10 mg/kg every 8 h. Furthermore, stent angioplasty was performed in coronary arteries of 16 minipigs: group 3 (n = 5, nine stents) = 100 U/kg heparin only; group 4 (n = 5, 10 stents) = 1-mg/kg bolus hirudin before and 45 min after angioplasty; group 5 (n = 6, 11 stents) = hirudin (1-mg/kg intravenous bolus) before and 45 min after angioplasty, followed by 6 to 10 mg/kg subcutaneously every 8 h. RESULTS: In segments with deep arterial injury, the number of platelets/angioplasty segment in group 2 after 72 h (mean 21, range 9.7 to 39.7 x 10(6)) was significantly less than that in group 1 (mean 375, range 72 to 787 x 10(6)). Morphometric analysis after 4 weeks showed no difference between groups in degree of vessel wall injury. Mean (+/- SD) neointimal thickness was 0.70 +/- 0.06 mm in group 3 and was significantly reduced in both group 4 (0.46 +/- 0.11 mm) and group 5 (0.48 +/- 0.21 mm). CONCLUSIONS: The direct thrombin inhibitor hirudin significantly reduces platelet deposition up to 72 h after coronary stent angioplasty. A hirudin bolus alone as well as continued subcutaneous administration for 14 days substantially reduced neointimal proliferation compared with heparin 4 weeks after coronary stent angioplasty in minipigs.

Platelet and fibrin deposition on coronary stents in minipigs: effect of hirudin versus heparin.

OBJECTIVES: The present study was designed to test the hypothesis that the direct thrombin hirudin is more efficient than heparin in reducing thrombus formation after coronary stenting. BACKGROUND: Despite aggressive anticoagulation, subacute thrombosis of coronary stents is a major complication associated with these new devices. METHODS: In 19 minipigs indium-111-labeled thrombocytes and iodine-125-labeled fibrinogen were injected 14 to 19 h before coronary implantation of tantalum balloon-expandable stents. In group 1 (n = 6, seven stents), a bolus of heparin (100 U/kg body weight) was given before stenting. Group 2 (n = 6, 11 stents) received both dextran (500 ml) and heparin (a 100-U/kg bolus followed by a continuous infusion of 50 U/kg per h). In group 3 (n = 7, 13 stents), hirudin (recombinant desulphatohirudin HV 1 [CGP 39393] [1 mg/kg]) was given before stent implantation, followed by an infusion of 1 mg/kg per h. All animals were pretreated with aspirin (250 mg intravenously). RESULTS: Activated partial thromboplastin time was prolonged to > 1.8 times control values in groups 2 and 3. Histologic examination after perfusion fixation 12 h after stenting showed a variable extent of thrombus on all stents. Medial tear was observed in three stents in group 1, six stents in group 2 and six stents in group 3. The number of platelets on all stents averaged 116.2 (range 22 to 522) x 10(6) in group 1, 64.3 (range 11 to 169) x 10(6) in group 2 and 19.7 (range 9 to 38) x 10(6) in group 3 (p < 0.05 vs. group 1 and vs. group 2). The increase in platelet deposition, associated with medial tear in all groups, was lowest in the hirudin group. Similarly, fibrin deposition was lowest on stents in hirudin-treated animals. CONCLUSIONS: Recombinant hirudin significantly reduces platelet and fibrin deposition on coronary stents compared with the reduction achieved with combined heparin, dextran and aspirin.

Expression of meta-vinculin in human coronary arteriosclerosis is related to the histological grade of plaque formation.

In the present study we demonstrate that the quantitative reduction of meta-vinculin expression parallels histological changes during the course of coronary arteriosclerosis. Immunofluorescence stainings of coronary arteries revealed that vinculin distribution resembled that of other smooth muscle-specific cytoskeletal proteins like alpha-actin, caldesmon or myosin light chain kinase in labeling smooth muscle cells brightly. Although close to arteriosclerotic plaques, the cellularity as measured by the density of nuclei was often not significantly altered. Cells of this location expressed markedly reduced amounts of vinculin, suggesting that they are smooth muscle cells of a synthetic phenotype. To determine the fractional meta-vinculin content in arteriosclerotic lesions, we performed densitometric scanning of immunoblots incubated with anti-vinculin monoclonal antibodies reacting with both meta-vinculin (150 kDa) and vinculin (130 kDa). In parallel, each tissue sample was evaluated histologically for the degree of arteriosclerotic alterations according to the morphometric atheroma score of Stratford et al. (n = 13). In type 1 lesions covering slight intimal thickening, meta-vinculin represented 36% (mean, range 35%-39%) of the total vinculin immunoreactivity. In type 2 lesions consisting of fibrous plaques of up to twice the original artery wall thickness, meta-vinculin accounted for 28% (mean, range 22%-35%) of the total vinculin content. Meta-vinculin was substantially reduced in type 3 lesions (mean 13%, range 8%-18%) which are characterized by extensive atheromatous plaques. Thus, the meta-vinculin/vinculin ratio differed significantly between early, intermediate and advanced phases of coronary arteriosclerotic plaque formation.

Accumulation of unphosphorylated calponin in the submembranous cytoskeletons of arachidonic acid-stimulated human platelets.

Calponin, a basic smooth-muscle protein capable of binding to F-actin, tropomyosin and calmodulin in vitro, was tested for its expression and subcellular localization in resting and stimulated human platelets. Using immunoblotting techniques calponin was revealed as a single protein band with a molecular weight of 34 kDa. Although calponin has been shown to be proteolytically degraded by calpain, in the presence of the calpain inhibitor E-64 and EGTA a significant hydrolysis of calponin could not be detected. Upon stimulation with 10 microM arachidonic acid calponin became increasingly incorporated into Triton X-100 insoluble cytoskeletal fractions reaching a plateau after 15 s. The accumulation of calponin in the cytoskeletons of stimulated platelets paralleled the polymerization of actin into newly formed microfilaments. Immunofluorescence microscopy revealed a submembranous co-localization of calponin and actin in aggregated platelets. Since isolated calponin is phosphorylated by protein kinase C and Ca2+/calmodulin-dependent protein kinase II thereby losing its inhibitory effect on the actomyosin MgATPase activity, we examined whether changes in cell shape due to platelet stimulation are accompanied by a phosphorylation of calponin. By performing immunoblotting analysis on either resting or stimulated platelets phosphorylation of calponin on tyrosine, serine or threonine residues could not be demonstrated. In line, [32P]radiolabeling experiments were unable to detect phosphate incorporation into calponin. These observations support the hypothesis that calponin plays a physiological role in regulating contraction and secretion of human platelets even in the absence of its phosphorylation.

Acute effects of the new angiotensin converting enzyme inhibitor ramipril on hemodynamics and carotid sinus baroreflex activity in congestive heart failure.

The hemodynamic effects of a single dose of 5 mg of ramipril, a new angiotensin converting enzyme inhibitor, were investigated in 10 patients with chronic congestive heart failure. Arterial blood pressure and total peripheral resistance were decreased by approximately 12% without causing reflex tachycardia. A highly significant decrease occurred in mean pulmonary artery and pulmonary capillary wedge pressures. These hemodynamic changes were equally pronounced at rest and during exercise on a bicycle ergometer; the effect was of the same magnitude 5 and 24 hours after medication. Angiotensin converting enzyme activity in plasma was nearly completely inhibited after 5 hours and remained at about 12% of control after 24 hours. Cardiac index, which was normal before treatment, remained unaffected. Thus, ramipril induced a balanced reduction of left ventricular pre- and afterload. The activity of the carotid sinus baroreflex was investigated in 8 of the patients using the neck suction technique before and 24 hours after ramipril. The reflex bradycardia during stimulation of the baroreceptors was significantly increased by ramipril, whereas the decrease in blood pressure remained essentially unaffected. Ramipril induced a selective sensitization of the parasympathetic baroreceptor heart rate reflex without influencing the sympathetically mediated peripheral vasodilatation. This effect may be responsible for the lack of reflex tachycardia in spite of the decrease in blood pressure.

On the necessity of the invasive predischarge test after implantation of a cardioverter-defibrillator.

The necessity of routine invasive implantable cardioverter-defibrillator (ICD) testing before hospital discharge was analyzed in 268 patients. In 98% of the patients, invasive ICD testing was not necessary if a preimplant electrophysiologic test was performed; most of the observed problems can be solved by noninvasive control.

Recanalization of chronic total coronary arterial occlusions by percutaneous excimer-laser and laser-assisted angioplasty.

A low primary success and high restenosis rate after recanalization of chronic total occlusions by conventional coronary angioplasty have encouraged the application of new interventional techniques like excimer-laser angioplasty. In 39 patients with a coronary occlusion for 1 to 12 months, recanalization was attempted by laser angioplasty through a multifiber-catheter coupled to a pulsed XeCl excimer laser. After successful passage of the occlusion by a standard guidewire in 27 patients (69%), the laser catheter was advanced over the central guidewire and crossed the occlusion in 25 patients (64%). In 2 patients with unsuccessful passage of the laser catheter, the subsequent attempt with a low profile balloon catheter also failed. In 19 of the 25 patients with successful laser recanalization, the residual stenosis exceeded 50% and was therefore followed by additional balloon angioplasty. The average residual stenosis after laser was 61 +/- 17% of the vessel diameter, and after balloon angioplasty 28 +/- 9% (n = 19), whereas after laser angioplasty alone it was 38 +/- 5% (n = 6). No complications associated with the laser application were observed. Angiographic control after 24 hours showed a reocclusion of 2 (8%) recanalized vessels. In this pilot study, laser angioplasty proved to be a safe and feasible method for the treatment of chronic total coronary occlusions. Because it was necessary to guide the catheter by a central wire, the primary success was limited by a successful passage of the wire of the occlusion. The rate of stand-alone laser angioplasty has to be increased by future improvements of the technique to enable a comparative evaluation of this method with conventional angioplasty.

Early detection of lead fracture by painless high voltage lead impedance measurement in a transvenous ICD lead system.

We report the case of a 69 year old patient, who underwent transvenous implantable cardioverter defibrillator (ICD) device change (Medtronic GEM VR 7227 Cx Active Can) because the ICD reached its replacement indicators. Preoperative chest X-ray and intraoperative defibrillation threshold tests and high voltage impedance did not show lead fracture of the five year old lead (Transvene 6936-65). At the second postoperative day the alarm of the newly implanted ICD device was activated because of high impedance in the painless lead impedance measurement (PLI) and the lead was replaced. The explanted lead showed a fracture detectable only by PLI.

Automatic atrial anti-tachy pacing for the termination of spontaneous atrial tachyarrhythmias: clinical experience with a novel dual-chamber pacemaker.

UNLABELLED: Automatic atrial anti-tachy pacing (aATP) is a novel approach to treat paroxysmal/persistent atrial tachyarrhythmias in pacemaker patients. To evaluate the efficacy of aATP in terminating spontaneous atrial flutter/tachycardia episodes (AT), a dual-chamber stimulator with extensive diagnostic capabilities and programmable aATP therapies (AT500(TM), Medtronic Inc.) was implanted in 30 patients with conventional pacing indications. During a mean follow-up time of 5.5 (1-12) months, aATP was delivered for 10494 AT. According to automatic device analysis, 8289 AT were treated with success (success-rate 79.0%). On 468 AT stored with the corresponding atrial EGM, an additional manual analysis was performed. The success-rate based on automatic analysis of these AT episodes (73.1%) was comparable to that found for all treated AT (79.0%), but manual EGM analysis revealed that only 209 of the 468 treated AT episodes (44.7%) were actually terminated by aATP. The aATP success-rate in the slower (cycle length 360-270 ms) AT detection zone was significantly higher (73.8%, 62/84 eps) than in the overlapping, faster (cycle length 270-220 ms) AT zone (38.3%, 147/384 eps, P<0.01). CONCLUSIONS: According to manual analysis, 1. aATP was safe and had a success-rate of 44.7%, 2. aATP success-rate was higher for AT in the slower than in the faster detection zone and 3. automatic analysis overestimated the efficacy of aATP.

Traumatic thrombosis of the left main coronary artery and myocardial infarction caused by blunt chest trauma.

We report the case of a 38-year-old man who, after a blunt chest trauma, developed an acute transmural myocardial infarction. Coronary arteriography revealed a thrombus in the left main artery, occlusion of the distal left anterior descending artery, and a diagonal branch caused by emboli.

Malignant restenosis after primary successful excimer laser coronary angioplasty.

In a series of 20 coronary excimer laser angioplasties, two patients presented with a peculiar type of malignant restenosis 6 and 8 weeks after a successful laser angioplasty procedure. One patient had a successful recanalization of an occluded left anterior descending (LAD) coronary artery and the second patient had a successful angioplasty of a subtotal proximal stenosis of the left anterior descending coronary artery. After the procedure, no ischemia could be demonstrated by exercise ECG and thallium scintigraphy. Both patients were free of angina until the sudden development of nocturnal angina several hours before reangiography, which showed subtotal restenosis in both cases. One patient had a mammaria graft on the LAD and the second patient underwent a successful balloon angioplasty. This uncommon sudden and malignant development of restenosis seems to be related to the excimer laser angioplasty procedure and warrants some caution with the indiscriminative use of this new angioplasty procedure.

Efficacy of balloon valvuloplasty in patients with critical aortic stenosis and cardiogenic shock--the role of shock duration.

BACKGROUND: Because of limited long-term success, aortic balloon valvuloplasty is considered to be a palliative procedure, including patients at excessive risk for standard therapy-aortic valve replacement-that is, those in cardiogenic shock. HYPOTHESIS: The study was undertaken to evaluate the outcome of balloon valvuloplasty for critical aortic stenosis complicated by cardiogenic shock. METHODS: Over a 10-year-period, we followed 14 patients (age 74+/-11 years, range 50-91) presenting in cardiogenic shock and critical aortic stenosis, who underwent valvuloplasty, together with 19 patients with critical aortic stenosis requiring urgent major noncardiac surgery. RESULTS: In patients in shock, calculated aortic valve area could be increased successfully by at least 0.3 cm2, from 0.38+/-0.09 to 0.81+/-0.12 cm2, with an insignificant increase in cardiac index from 1.89+/-0.33 to 2.01+/-0.41 l/min * m2. In-hospital mortality was 71% (10 patients). Two patients underwent valve replacement within 16 days and survived after 1 year, as did two patients refusing surgery. By multivariate logistic regression analysis, only an interval between onset of shock symptoms and valvuloplasty of > 48 h was significantly associated with fatal outcome (p < 0.01). In those patients requiring noncardiac surgery, this was possible after valvuloplasty in 95% who survived 1 year after hospital discharge. One patient in this group died of pulmonary embolism the day after the procedure. CONCLUSION: These data support the concept of causal treatment in patients with cardiogenic shock, as well as in the setting of cardiogenic shock and critical aortic stenosis, at the earliest possible convenience.

Cutting balloon coronary angioplasty--initial clinical experience.

The success of percutaneous transluminal coronary angioplasty is limited by acute occlusion and late restenosis. In 25 patients (20 men, 5 women, age range 36-81 years) coronary angioplasty was performed using a new cutting balloon into which 3-4 longitudinally orientated blades are incorporated so as to reduce the rate of severe dissections. In 12 patients stenoses were reduced from 83.9 +/- 7.8% to 28.4 +/- 10.7% (mean +/- SD) by the cutting balloon alone, using predilatation with a small conventional balloon in two cases. Thirteen other patients were additionally dilated with a conventional balloon because of a residual stenosis > 50% after cutting balloon angioplasty. Here the stenoses could be reduced from 78.1 +/- 8.7% to 29.1 +/- 11.3%. Six months follow-up angiography in 14 patients showed > 50% restenosis in two of seven patients dilated with a conventional balloon in addition to the cutting balloon, and in one of seven patients dilated with the cutting balloon alone but predilated with a small conventional balloon. These results show that coronary angioplasty by the new cutting balloon results in a stenosis reduction comparable with conventional balloons at a low complication rate. Available 6 months follow-up data show three restenoses in patients either pre- or postdilated by a conventional balloon and none in stand-alone cutting balloon cases.

Initial clinical results with the Wiktor stent: a new balloon-expandable coronary stent.

The Wiktor stent, a new coronary balloon-expandable tantalum stent, was implanted in 17 patients for other wise nonmanageable occlusion after balloon angioplasty (n = 11) and for recurrent restenosis (n = 6). Stents of 3.0 to 4.0 mm were implanted (right coronary artery: n = 10, left anterior descending artery: n = 4, left circumflex artery: n = 2, venous graft: n = 1). All patients were fully anticoagulated initially with heparin followed by coumadin for 3 months and were treated with acetylsalicylic acid indefinitely. Due to its good radiopacity, the device could be placed easily without complications. Early occlusion occurred in one patient after 8 h probably due to friable atheromatous material prolapsing between the meshes of the stent. Late occlusion occurred in another patient who was admitted in cardiogenic shock after pre-hospital reanimation and was stented after occlusive disection following balloon angioplasty of an occluded right coronary artery. In this patient with severe hypoxic brain damage, reocclusion and reinfarction to which the patient finally succumbed occurred following cessation of anticoagulation. Histology demonstrated occlusive thrombosis without evidence of a neointimal covering of the stent. Another thrombotic occlusion due to inadvertent omission of anticoagulation occurred in another patient two weeks after stenting. Control angiography after 6 months in 12 patients revealed restenosis in two patients (50% and 80%). The patient with 80% restenosis of the right coronary artery and pathologic results during stress testing underwent surgical revascularization. The other patient with a 50% restenosis of the right coronary artery was managed medically as he was asymptomatic and without evidence of ischemia during stress testing.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary angioplasty in patients with previous coronary artery bypass grafting.

Between 1982 and 1990, in 134 patients with prior coronary artery bypass grafting and recurrent angina, repeat coronary angiography and balloon angioplasty of stenoses in grafts or native arteries were attempted. Mean age of grafts was 45.6 months, range three days to twelve years. At the time of angioplasty, 6 patients had one-vessel-disease, 33 had two-vessel-disease, and 95 had three-vessel-disease. A total of 182 lesions were dilated: 55 venous grafts, 3 internal mammary artery grafts, and 124 native vessels. Forty-nine of 55 (89%) venous grafts could be successfully dilated, and in 3 internal mammary artery grafts, a stenosis reduction greater than 50% was achieved. In 65 of 88 (74%) grafted native arteries, dilation success was achieved. Twenty-seven of 36 (75%) patients with prior bypass surgery to other arteries had successful angioplasty of nongrafted native arteries. Three patients underwent emergency bypass surgery after dissection and acute occlusion: one of them died in cardiogenic shock secondary to acute myocardial infarction. The angiographic success rate in grafts was slightly higher than in native arteries (90% vs 74%). These data indicate that percutaneous transluminal coronary angioplasty in patients after bypass surgery is possible at a low risk (3%) and constitutes an effective therapy in symptomatic patients.

[The renin-angiotensin system in cardiovascular diseases]. / Das Renin-Angiotensin-System bei kardiovaskulären Erkrankungen.

BACKGROUND: The renin-angiotensin system is mainly involved in several cardiovascular diseases and in the pathophysiology of heart failure. It exists as a circulating and a local system which can be differently regulated. Interventions in this system by angiotensin-converting enzyme (ACE) antagonists or angiotensin-receptor antagonists slow the progression of heart failure and result in prolongation of life expectancy and improvement of hemodynamics. MECHANISMS OF ACTION: The main underlying mechanisms are: 1. Heart failure results in activation of the renin-angiotensin system as a compensatory mechanism with elevation of circulating angiotensin II, norepinephrine and vasopressin. Antagonists of this compensatory mechanisms acutely result in improvement of the hemodynamic situation. 2. Elevated circulating and local renin-angiotensin systems cause chronic structural myocardial and vascular effects. Angiotensin-converting enzyme antagonists and angiotensin-receptor blockers modulate and partly antagonize these structural changes such as myocardial hypertrophy, myocardial fibrosis and vascular proliferative responses. Gene and receptor regulation of the system are currently not fully understood and are subject of intensive research. 3. The renin-angiotensin system is closely related to the bradykinin system and thus indirectly to nitric oxide and endothelial function. Bradykinin has multiple other effects on the hemostatic system as a well as on the myocardium and vascular system. CONCLUSION: These complex interactions require further evaluation. Research with specific bradykinin antagonists will give new insights into this system.

[Acute effects of the angiotensin converting enzyme inhibitor ramipril in patients with coronary heart disease]. / Akute Effekte des Angiotensin-Converting-Enzym-Hemmers Ramipril bei Patienten mit koronarer Herzerkrankung.

We investigated the acute effect of the new long-acting ACE-inhibitor ramipril on angina-limited exercise tolerance and exercise-induced ST-depression in 18 normotensive patients with angiographically confirmed coronary artery disease in a double-blind, placebo-controlled study. Patients underwent a repeat exercise ECG 24 hours following either 5 mg ramipril p.o. or placebo. Plasma-ACE activity (nmol/min x ml) in the ramipril-group (n = 8) was significantly reduced 24 hours after 5 mg ramipril compared to placebo (n = 10): 14.0 +/- 2.0 vs 87.2 +/- 13.5, p less than 0.001. Exercise-induced ST-segment depression was not different before and after ramipril or placebo. Heart rate at rest and during angina-limited exercise was not different between the first exercise-ECG and that after ramipril or placebo, nor between the groups. Systolic arterial pressure (mmHg) was slightly, but insignificantly, lower after than before ramipril at rest (113.8 +/- 5 vs 125 +/- 6.8) and at maximal exercise, 1.5 watt/kg (150 +/- 9.4 vs 158.3 +/- 13.3). In the placebo group, blood pressure at rest and during exercise was not different before and after placebo: 126 +/- 4.7 vs 125.5 +/- 7.5 and 157.5 +/- 3.8 vs 158 +/- 3.6. Rate-pressure-product (mmHg/min x 1000) at rest prior to (8.42 +/- 0.83 and 8.95 +/- 0.51) and after ramipril or placebo (8.00 +/- 0.94 and 8.93 +/- 0.71) showed no significant difference. Similarly, rate-pressure-product at maximal exercise was equal among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Structures and rearrangement reactions of 4-aminophenol(H2O)1+ and 3-aminophenol(H2O)1+ clusters.

In this paper the structures of 4-aminophenol(H2O)1+ and 3-aminophenol(H2O)1+ clusters are investigated in molecular beam experiments by different IR/UV-double resonance techniques as well as the mass analyzed threshold ionization spectroscopy yielding both inter- and intramolecular vibrations of the ionic and neutral species. Possible structures are extensively calculated at the level of density functional theory (DFT) or at the ab initio level of theory. From the experimental and theoretical investigations it can be concluded that in the case of 4-aminophenol(H2O)1 one O-H...O hydrogen-bonded structure exists in the neutral cluster but two structures containing either an O-H...O or a N-H...O hydrogen-bonded arrangement are observed in the spectra of the ionic species. This observation is a result of an intramolecular rearrangement reaction within the ion which can only take place if high excess energies are used. A reaction path via the CH bonds is calculated and explains the experimental observations. In the case of 3-aminophenol(H2O)1+ only one O-H...O bound structure is observed both in the neutral and ionic species. Ab initio and DFT calculations show that due to geometrical and energetical reasons a rearrangement cannot be observed in the 3-aminophenol(H2O)1+ cluster ion.