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P Hanrath

Publications and source records attributed to P Hanrath.

At least 109 records · Page 6Linked to original sources
PubMed1999

Clinical and angiographic predictors of recurrent restenosis after percutaneous transluminal rotational atherectomy for treatment of diffuse in-stent restenosis.

Due to the widespread use of stents in complex coronary lesions, stent restenosis represents an increasing problem, for which optimal treatment is under debate. "Debulking" of in-stent neointimal tissue using percutaneous transluminal rotational atherectomy (PTRA) offers an alternative approach to tissue compression and extrusion achieved by balloon angioplasty. One hundred patients (70 men, aged 58 +/- 11 years) with a first in-stent restenosis underwent PTRA using an incremental burr size approach followed by adjunctive angioplasty. The average lesion length by quantitative angiography was 21 +/- 8 mm (range 5 to 68) including 22 patients with a length > or = 40 mm. Twenty-nine patients had complete stent occlusions with a lesion length of 44 +/- 23 mm. Baseline diameter stenosis measured 78 +/- 17%, was reduced to 32 +/- 9% after PTRA, and further reduced to 21 +/- 10% after adjunctive angioplasty. Primary PTRA was successful in 97 of 100 patients. Clinical success was 97%, whereas 2 patients developed non-Q-wave infarctions without clinical sequelae. Clinical follow-up was available for all patients at 5 +/- 4 months without any cardiac event. Angiography in 72 patients revealed restenosis in 49%, with necessary target lesion reintervention in 35%. The incidence of rerestenosis correlated with the length of the primarily stented segment and the length of a first in-stent restenosis. Thus, PTRA offers an alternative approach to treat diffuse in-stent restenosis. Neointimal debulking of stenosed stents can be achieved effectively and safely. PTRA resulted in an acceptable recurrent restenosis rate in short and modestly diffuse lesion, whereas the restenosis rate in very long lesions remains high despite debulking.

Atherectomy, Coronary↗
PubMed1999

Influence of a platelet GPIIb/IIIa receptor antagonist on myocardial hypoperfusion during rotational atherectomy as assessed by myocardial Tc-99m sestamibi scintigraphy.

OBJECTIVES: This study evaluated the effect of the glycoprotein IIb/IIIa (GPIIb/IIIa) antagonist abciximab on myocardial hypoperfusion during percutaneous transluminal rotational atherectomy (PTRA). BACKGROUND: PTRA may cause transient ischemia and periprocedural myocardial injury. A platelet-dependent risk of non-Q-wave infarctions after directional atherectomy has been described. The role of platelets for the incidence and severity of myocardial hypoperfusion during PTRA is unknown. METHODS: Seventy-five consecutive patients with complex lesions were studied using resting Tc-99m sestamibi single-photon emission computed tomography prior to PTRA, during, and 2 days after the procedure. The last 30 patients received periprocedural abciximab (group A) and their results were compared to the remaining 45 patients (group B). For semiquantitative analysis, myocardial perfusion in 24 left ventricular regions was expressed as percentage of maximal sestamibi uptake. RESULTS: Baseline characteristics did not differ between the groups. Transient perfusion defects were observed in 39/45 (87%) patients of group B, but only in 10/30 (33%) patients of group A (p < 0.001). Perfusion was significantly reduced during PTRA in 3.3 +/- 2.5 regions in group B compared to 1.4 +/- 2.5 regions in group A (p < 0.01). Perfusion in the region with maximal reduction during PTRA in groups B and A was 76 +/- 15% and 76 +/- 15% at baseline, decreased to 56 +/- 16% (p < 0.001) and 67 +/- 14%, respectively, during PTRA (p < 0.01 A vs. B), and returned to 76 +/- 15% and 80 +/- 13%, respectively, after PTRA. Nine patients in group B (20%) and two patients in group A (7%) had mild creatine kinase and/or troponin t elevations (p = 0.18). Patients with elevated enzymes had larger perfusion defects than did patients without myocardial injury (4.2 +/- 2.7 vs. 2.3 +/- 2.5 regions, p < 0.05). CONCLUSIONS: These data indicate that GPIIb/IIIa blockade reduces incidence, extent and severity of transient hypoperfusion during PTRA. Thus, platelet aggregation may play an important role for PTRA-induced hypoperfusion.

Abciximab↗
PubMed1999

Potential benefit of biventricular pacing in patients with congestive heart failure and ventricular tachyarrhythmia.

Treatment of congestive heart failure (CHF) aims for symptomatic relief and reduction of mortality both from sudden death and pump failure. The implantable cardioverter defibrillator (ICD) is highly effective in the prevention of sudden death, but no mortality benefit in advanced CHF has yet been shown. Biventricular pacing may lead to functional improvement in selected patients with CHF. Thus, a biventricular pacemaker with defibrillation capabilities may be ideal for patients with advanced CHF. We retrospectively analyzed the data from 384 patients (age 59 +/- 12 years, 322 male and 62 female) with regard to New York Heart Association (NYHA) CHF class, mean QRS duration, mean PR interval, presence of a QRS > 120 msec and incidence of atrial fibrillation at the time of ICD implantation. Based on eligibility criteria from studies in biventricular pacing, we analyzed how many patients may benefit from biventricular pacing. Patients with CHF were older (NYHA class III: 60.9 +/- 9.7, class II: 61.3 +/- 10 versus class I: 50.8 +/- 13.6 years, p < 0.001 each) and mean QRS duration was longer with advanced CHF (NYHA class III 127.8 +/- 30 msec; class II 119.4 +/- 27.7 msec; class 0-1: 103.9 +/- 17.7 msec, p < 0.001, analysis of variance) as was the mean PR interval (NYHA class III 189.9 +/- 33.5 msec; class II 176.1 +/- 29.3 msec; class 0-1 162.7 +/- 45.9 msec, p < 0.001, analysis of variance). The incidence of atrial fibrillation was higher in class III (25.5%) compared with class 0-1 (16.9%) and class II patients (14.1%, p = 0.043, chi-square test). A total of 28 patients (7.3%) fulfilled eligibility criteria for biventricular pacing if NYHA class III patients were considered candidates and 48 (12.5%) if patients with NYHA II CHF and ejection fraction < or = 30% were included. Thus, biventricular pacing may offer a promising therapeutic approach for a significant proportion of patients with CHF at risk for ventricular tachyarrhythmia.

Aged↗
PubMed1999

Reduced myocardial sarcoplasmic reticulum Ca(2+)-ATPase protein expression in compensated primary and secondary human cardiac hypertrophy.

Pathological intracellular calcium handling has been proposed to underlie the alterations of contractile behavior in hypertrophied myocardium. However, the myocardial protein expression of intracellular calcium transport proteins in compensated human left ventricular hypertrophy has not yet been studied. We investigated septal myocardial specimens of patients suffering from hypertrophic obstructive cardiomyopathy (n=14) or from acquired aortic valve stenosis (n=11) undergoing myectomy or aortic valve replacement, respectively. For comparison, we studied non-hypertrophied myocardium of six non-failing hearts which could not be transplanted for technical reasons. The myocardial density of the calcium release channel of the sarcoplasmic reticulum (SR) was determined by(3)H-ryanodine binding. Myocardial contents of SR Ca(2+)-ATPase, phospholamban, calsequestrin and Na(+)/Ca(2+)-exchanger were analysed by Western blot analysis. The myocardial SR calcium release channel density was not significantly different in hypertrophied and non-failing human myocardium. In both hypertrophic obstructive cardiomyopathy and in aortic valve stenosis, SR Ca(2+)-ATPase expression was reduced by about 30% compared to non-failing myocardium (P<0.05), whereas the expression of phospholamban, calsequestrin, and the Na(+)/Ca(2+)-exchanger was unchanged. The decrease of SR Ca(2+)-ATPase expression was still observable when related to its regulatory protein phospholamban or to the myosin content of the homogenates (P<0.05). Furthermore, the SR Ca(2+)-ATPase expression was inversely correlated to the septum thickness assessed by echocardiography, but not to age, cardiac index or outflow tract gradient. In primary as well as in secondary hypertrophied human myocardium, the expression of SR Ca(2+)-ATPase is reduced and inversely related to the degree of the hypertrophy. The diminished SR Ca(2+)-ATPase expression might result in reduced Ca(2+)reuptake into the SR and might contribute to altered contractile behavior in hypertrophied human myocardium.

Adult↗
PubMed1999

[Cardiology].

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Adult↗
PubMed1999

Altered force-frequency relation in hypertrophic obstructive cardiomyopathy.

The present study was designed to test the hypothesis that in hypertrophied myocardium of patients with hypertrophic obstructive cardiomyopathy (HOCM) a reduced contractile reserve provided by frequency dependent potentiation of force of contraction contributes to the myocardial dysfunction. Myectomy was performed in 8 HOCM patients with normal systolic left ventricular function at rest. Nonfailing myocardium from the hearts of three multiorgan donors was investigated for comparison. In thin myocardial strips we measured the inotropic effects of different stimulation frequencies (0.5-3.0 Hz) at different extracellular Ca2+ concentrations (1.8-16.2 mmol/l). At 1.8 mmol/l extracellular Ca2+ concentration, increasing stimulation rates had no positive inotropic effect in HOCM myocardium, whereas in nonfailing myocardium force of contraction increased up to 3 Hz. Increasing extracellular Ca2+ concentrations induced a positive force-frequency relation in HOCM with a maximum at 5.4 mmol/l Ca2+. A further increase to 16.2 mmol/l Ca2+ resulted in a negative force-frequency relation in these specimens. The time to peak tension and the time to relaxation decreased at increasing stimulation frequencies at all Ca2+ concentrations investigated. In conclusion, in hypertrophied myocardium of HOCM patients increasing stimulation frequencies failed to have a positive inotropic effect at physiological extracellular Ca2+ concentrations. The induction of a positive force-frequency relation by higher Ca2+ concentrations suggests that an abnormal cellular Ca2+ handling may play an important pathophysiological role.

Calcium↗
PubMed1999

Calcium-sensitivity of the SR calcium release channel in failing and nonfailing human myocardium.

BACKGROUND: Altered Ca2+ metabolism of the sarcoplasmic reticulum results in changes of the contractile behavior in failing human myocardium. The ryanodine-sensitive Ca2+ release channel of the sarcoplasmic reticulum plays a key role in the intracellular Ca2+ handling in cardiac myocytes. Recently, we showed that the density of 3H-ryanodine binding sites which correspond to the SR Ca2+ release channel in human myocardial homogenates is unchanged in failing human myocardium. However, the sensitivity of the channel towards Ca2+, which acts as the trigger signal of channel activation and thereby initiates contraction, has not yet been investigated in failing and nonfailing myocardium. METHODS: Homogenates (100 micrograms protein) from hearts with dilated (DCM, n = 10) or ischemic (ICM, n = 9) cardiomyopathy were incubated with a saturating concentration of 3H-ryanodine (12 nM) in the presence of different Ca2+ concentrations ranging from 1 nM to 10 mM. For comparison, myocardium of 8 nonfailing hearts which could not be transplanted for technical reasons was investigated. Non-specific binding was determined in the presence of a high concentration (10 microM) of unlabeled ryanodine. RESULTS: 3H-ryanodine binding to the Ca2+ release channel showed a bell-shaped pattern with an increase in specific binding at submicromolar Ca2+ concentrations and a decrease at higher Ca2+ concentrations than 0.5 mM, whereas nonspecific binding was not influenced by different Ca2+ concentrations. In nonfailing myocardium, maximal 3H-ryanodine binding (Bmax) was 85.2 +/- 3.1 fmol/mg protein and half-maximal binding was reached at a free Ca2+ concentration of 0.25 (0.22-0.30) microM (EC50). Neither EC50 values nor maximal specific 3H-ryanodine binding differed between nonfailing and failing myocardium of both etiologies. EC50 values were 0.24 (0.23-0.26) microM (DCM, n = 10) or 0.28 (0.25-0.31) microM (ICM, n = 9), respectively. Caffeine (2 mM) and the ATP-analogon AMP-PCP (1 mM) led to a shift towards lower Ca2+ concentrations consistent with an activation of the channel by these compounds, whereas Mg2+ (0.7 mM) shifted the Ca(2+)-dependence of 3H-ryanodine binding towards higher Ca2+ concentrations indicating inhibition of channel opening. After activation of the Ca2+ release channel by caffeine or AMP-PCP as well as after the inhibition with Mg2+ EC50 values were the same in failing and nonfailing myocardium. CONCLUSION: Caffeine and AMP-PCP sensitize, whereas Mg2+ desensitizes the myocardial Ca2+ release channel to Ca2+. The determination of Ca(2+)-dependent 3H-ryanodine binding to the human myocardial Ca2+ release channel is a useful tool to investigate its open probability. Furthermore, the Ca(2+)-sensitivity and the pharmacological behavior of the human SR Ca2+ release channel are similar in failing and nonfailing myocardium.

Calcium↗
PubMed1999

Mechanisms of acute lumen gain and recurrent restenosis after rotational atherectomy of diffuse in-stent restenosis: a quantitative angiographic and intravascular ultrasound study.

OBJECTIVES: This quantitative angiographic and intravascular ultrasound study determined the mechanisms of acute lumen enlargement and recurrent restenosis after rotational atherectomy (RA) with adjunct percutaneous transluminal coronary angioplasty in the treatment of diffuse in-stent restenosis (ISR). BACKGROUND: In-stent restenosis remains a significant clinical problem for which optimal treatment is under debate. Rotational atherectomy has become an alternative therapeutic approach for the treatment of diffuse ISR based on the concept of "tissue-debulking." METHODS: Rotational atherectomy with adjunct angioplasty of ISR was used in 45 patients with diffuse lesions. Quantitative coronary angiographic (QCA) analysis and sequential intravascular ultrasound (IVUS) measurements were performed in all patients. Forty patients (89%) underwent angiographic six-month follow-up. RESULTS: Rotational atherectomy lead to a decrease in maximal area of stenosis from 80+/-32% before intervention to 54+/-21% after RA (p < 0.0001) as a result of a significant decrease in intimal hyperplasia cross-sectional area (CSA). The minimal lumen diameter after RA remained 15+/-4% smaller than the burr diameter used, indicating acute neointimal recoil. Additional angioplasty led to a further decrease in area of stenosis to 38+/-12% due to a significant increase in stent CSA. At six-month angiographic follow-up, recurrent restenosis rate was 45%. Lesion and stent length, preinterventional diameter stenosis and amount of acute neointimal recoil were associated with a higher rate of recurrent restenosis. CONCLUSIONS: Rotational atherectomy of ISR leads to acute lumen gain by effective plaque removal. Adjunct angioplasty results in additional lumen gain by further stent expansion and tissue extrusion. Stent and lesion length, severity of ISR and acute neointimal recoil are predictors of recurrent restenosis.

Aged↗
PubMed1999

Effects of lovastatin on progression of non-dilated and dilated coronary segments and on restenosis in patients after PTCA. The cholesterol lowering atherosclerosis PTCA trial (CLAPT).

OBJECTIVES: The Cholesterol Lowering Atherosclerosis PTCA Trial (CLAPT) is a prospective, randomized trial with blinded angiographic end-points to assess the effect of 2-year's treatment with lovastatin initiated 4 weeks prior to PTCA, compared to usual care on non-dilated coronary segments and on dilated coronary lesions in male patients with total cholesterol between 200 and 300 mg. dl(-1)who underwent elective PTCA. METHODS AND RESULTS: Two hundred and twenty six patients were randomized 4 weeks prior to PTCA to special care (diet plus lovastatin n=112) or usual care (diet; n=114). One hundred and ninety-nine patients underwent PTCA at baseline and were finally included in the study. Quantitative coronary angiographic assessment was performed on blinded cinefilms at baseline (PTCA) and repeated after 4 and 24 months in 91% and 81% of the patients. The primary end-point was a change in the mean segment diameter of non-dilated segments. The mean lovastatin dose was 33 mg. day(-1). Total- and LDL-cholesterol decreased by 21% and 29% in the special care group and by 7% and 11% in the usual care patients. After 2 years, the mean segment diameter of non-dilated segments decreased by 0.03 mm in the usual care group and 0.004 mm in the special care group (P=0.27). The decrease in the mean segment diameter of dilated lesions was 0.17 mm (usual care) and 0.06 mm (special care) (P=0.04) after 4 months; 0.16 mm (usual care) and 0. 002 mm (special care) after 24 months, respectively (P=0.05). In both groups, the mean segment diameter of dilated lesions increased between 4 and 24 months after PTCA compared to a decrease in mean segment diameter of non-dilated segments (P<0.05). Restenosis (>50% diameter stenosis at follow-up) occurred in 28.4% of usual care and 22.2% of special care patients (P=0.17). CONCLUSIONS: Lovastatin reduced the progression of dilated lesions in men with elective PTCA. Independent of treatment allocation, the dilated lesions regressed and the non-dilated segments progressed during the study follow-up. Four weeks of pre-treatment with lovastatin did not influence the rate of restenosis. Lovastatin had no statistically significant effect on non-dilated segments.

Angioplasty, Balloon, Coronary↗
PubMed1999

Extent and severity of test positivity during dobutamine stress echocardiography. Influence on the predictive value for coronary artery disease.

AIMS: Recent studies have evaluated the diagnostic accuracy and predictive value of dobutamine echocardiography without considering the additional information implied by the magnitude of induced wall motion abnormalities. We sought to evaluate the positive predictive value of dobutamine echocardiography for coronary artery disease from the extent and severity of the induced wall motion abnormality. In addition, we intended to determine factors associated with false-negative dobutamine echocardiography. METHODS AND RESULTS: Two hundred and eighty-three consecutive patients with suspected coronary artery disease underwent dobutamine echocardiography (up to 40 microg x kg(-1) x min(-1)+atropine up to 1 mg) and coronary angiography. The number of segments and the degree of deterioration were used to describe the extent and severity of induced wall motion abnormality. Analysis of clinical, procedural and echocardiographic variables was performed to determine factors associated with false-negative results. The positive predictive value of dobutamine echocardiography increased from 85% to 90%, 94% and 94% with deterioration of wall motion by one grade in >/=1, >/=2, >/=3 and >/=4 segments, respectively (P<0.05). Deterioration of wall motion by two grades in one segment had a positive predictive value of 96% as compared to 85% for deterioration by only one grade in one segment (P<0.05). Patients with false-negative test results received atropine more frequently (28% vs 13%, odds ration [OR]=3.87, 95% confidence interval [CI]=1.54-9.75, P=0.028) than patients with a correct positive result. However, angina (15 vs 37%, OR=0.26, 95% CI=0.09-0.71, P=0.010), ECG changes during dobutamine stress (15% vs 35%, OR=0.49, 95% CI 0.19-1.25, P=0.014) and high image quality (OR 1.59, 95% CI 1.07-2.37, P=0.015) were less frequent. The sensitivity of dobutamine echocardiography increased from 67% to 71% and 86% (P<0.05) with increasing achieved maximal heart rate (<75%, 75-85% and >85% of maximal heart rate). CONCLUSION: The positive predictive value of dobutamine echocardiography increases significantly as the extent and severity of induced wall motion abnormality increases. Thus, the degree of test positivity should be reported in clinical practice. Despite high pharmacological drug doses, the haemodynamic response may still be insufficient in some patients to induce myocardial ischaemia, resulting in false-negative dobutamine echo tests. To maximize the sensitivity of dobutamine echocardiography, the highest haemodynamic stress level, with a heart rate above 85% of the predicted heart rate, should be reached.

Adult↗
PubMed1999

Effect of nitroglycerin and nicorandil on regional poststenotic quantitative coronary blood flow in coronary artery disease: a combined digital quantitative angiographic and intracoronary doppler study.

Little information is available concerning the effects of nitrates and potassium channel openers on local poststenotic blood flow in coronary artery disease (CAD). Combined quantitative digital angiography (QCA) and intracoronary Doppler (IVADO) velocity measurements were used to determine changes in absolute poststenotic blood flow after intracoronary injection of 0.2 mg nitroglycerin and 0.5 mg nicorandil. Quantitative blood flow (QBF) was calculated from average peak-flow velocity (APV) and angiographic cross-sectional area (CSA): QBF (ml/min) = CSA x APV x 0.5. In group I (n = 9), 0.5 mg nicorandil i.c. was identified as optimal to achieve maximal vasodilatation. In patients with CAD (group II, n = 12), i.c. injection of 0.5 mg nicorandil induced a significant increase in poststenotic CSA (+38%) and QBF (+50%). In contrast, 0.2 mg nitroglycerin (group III, n = 12) increases poststenotic CSA (+38%) without a significant change in QBF (+23%). Additional application of nicorandil in these patients induced further significant increases in CSA (+55%) and QBF (+48%) compared with baseline. There were no significant changes in stenosis area. Poststenotic blood flow can be increased by nicorandil after application of nitroglycerin. This effect is most likely mediated by the potassium channel-opening effect of nicorandil. Combined use of QCA and IVADO is a unique approach to measure local poststenotic QBF in patients with CAD.

Coronary Angiography↗
PubMed1999

Optimized pulse durations minimize the effect of polarity reversal on defibrillation efficacy with biphasic shocks.

There are conflicting results on the effect of polarity change on the defibrillation efficacy of biphasic shocks possibly caused by different shock durations. The goal of the present study was to investigate the influence of polarity reversal on defibrillation efficacy for different biphasic shock durations in a porcine animal model. In eight anesthesized pigs using a transvenous/submuscular lead system DFTs for 4 phase 1 durations were determined: 8.1 ms, 6 ms, 3.8 ms and 1.7 ms. The phase 1/phase 2 ratio was constant at 60%/40%. For cathodal shocks, the defibrillation coil in the right ventricular apex was the cathode during phase 1 and for anodal shocks it was the anode. For both polarities, the strength-duration curve revealed a DFT minimum at 3.8 ms (cathodal shocks: 21.3 +/- 6.4 J, P < 0.001; anodal shocks: 21.9 +/- 8 J, P = 0.05). For anodal shocks and phase 1 durations of 1.7, 3.8, and 6 ms there was no significant difference of the stored energy at the DFT compared to cathodal shocks. In contrast, significantly lower DFTs were observed for anodal shocks with a phase 1 duration of 8.1 ms (28.8 +/- 6.4 J compared to 33.1 +/- 5.9 J for cathodal shocks, P = 0.006). The effect of lower defibrillation energy requirements with polarity reversal depends on the total biphasic shock duration; for the pulse duration with the lowest DFT, polarity reversal does not increase defibrillation efficacy of biphasic shocks.

Animals↗
PubMed1999

Hypoxic Hypoperfusion Fails to Induce Myocardial Hibernation in Anesthetized Swine.

BACKGROUND: Congenital origin of the left coronary artery from the pulmonary artery (ALCAPA) results in chronically dysfunctional myocardium with the partial ability to recover after revascularization. We attempted to establish an ALCAPA syndrome in anesthetized pigs for 24 hours and to compare it with stunned and infarcted myocardium. METHODS AND RESULTS: In group 1 (n = 12), a bypass graft was interposed between the pulmonary artery and the left anterior descending coronary artery (LAD). Reduction of flow in the LAD with gradual increases in flow from the pulmonary artery resulted in an incremental reduction of segment shortening (8.9 +/- 5.3% at 24 hours vs 26.6 +/- 10% at baseline, P <.005). In group 3 (n = 5), 2 cycles of 10-minute LAD occlusion resulted in decreased segment shortening with slow recovery (at 24 hours 18.7 +/- 1.3% vs 24.2 +/- 4% at baseline, segment shortening with slow recovery (at 24 hours 18.7 +/- 1.3% vs 24.2 +/- 4% at baseline, P <.05). In group 3 (n = 6), 1-hour LAD occlusion reduced segment shortening at 24 hours to 4.7 +/- 5.2% (P <.005 vs baseline). Histological analysis of the LAD territory revealed severe degeneration, myolysis, and alteration of the chromatin structure in group 1 comparable to ischemic cell death in group 3, whereas control areas and the LAD area in group 2 showed only minor structural alterations. Infarct size/risk area, as measured by tetrazolium staining, was 49.8 +/- 11.2% in group 1, 9.3 +/- 8.1% in group 2 (P <.005), and 60.3 +/- 9% in group 3. CONCLUSION: Hypoxic myocardial hypoperfusion from the pulmonary artery results in myocardial necrosis in anesthetized pigs. These findings are in contrast to the concept of myocardial hibernation in the ALCAPA syndrome because in this model, hypoxic hypoperfusion failed to induce adaptation to preserve myocardial structure.

Journal Article↗