No-reflow phenomenon is the absence of myocardial perfusion despite adequate dilatation of the infarct related coronary artery during percutaneous coronary intervention. It predicts severe left ventricular dysfunction and poor prognosis in acute myocardial in-farction (AMI). The present case is a 54 year old Turkish female who presented with chest pain that had started 2.5 hours earlier. The clinical and laboratory findings were consistent with AMI and the coronary angiogram performed for primary angioplasty revealed a 95% thrombotic occlusion with a TIMI grade I flow in the left anterior descending (LAD) coronary artery. A TIMI grade III flow was achieved with direct stent deployment. However, after the placement of a second stent for severe ostial stenosis more proximally and adjacent to the first one, the antegrade flow became TIMI grade O. As the intracoronary medications did not improve the flow, a mechanical occlusion was considered and a third stent was deployed covering the first two stents. A control angiogram revealed the persistence of TIMI grade O flow. A severe and persistent vasospasm was considered at this point and accordingly, intracoronary verapamil was administered in high concentrations by an infusion catheter to the distal LAD which was followed by the immediate achievement of TIMI grade III flow. Intracoronary administration of high dose verapamil can be performed to prevent vasospasm in resistant no-reflow cases with no evidence of mechanic occlusion.

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The long-term outcomes of coronary artery stenting have been determined by coronary angiography only with has the limitation of determining stent expansion and neointimal proliferation at long-term follow-up. Volumetric intravascular analysis has the potential to evaluate the morphology and distribution of neointima longitudinally after coronary artery stenting. We used three-dimensional intravascular ultrasound (3-D IVUS) to evaluate serial changes in stent and neointimal volumes for over 1-year in 9 patients who did not exhibit angiographic restenosis at 6-month follow-up. Volumetric analysis by a validated Netra 3-D IVUS system was performed pre- and post-intervention, at 6-month follow-up (FU1), and at over one-year follow-up (FU2). Lumen volume in the stented lesions increased significantly after intervention, and the increase persisted until FU2. There were no significant changes in stent volume between just after stent implantation and at FU2. Neointimal volume within the stents did not change from FU1 to FU2 (FU1; 38.4±9.0 mm³ vs FU2; 33.8±10.3 mm³). In 33% (3/9) of all lesions, neointimal volume increased between from 6-months to over 1-year after stent implantation. Neointimal distribution after stenting seemed to be almost equal and unrelated to the plaque burden at pre-intervention. Neointimal volume within the stents did not increase and stent volume did not change over the 1st-year in patients who did not exhibit angiographic restenosis at 6-months.

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The aim of this study was to assess the relations between inflammation, immune response, and coronary angiographic findings in patients with unstable angina pectoris (UAP).
Recent studies suggest a role for inflammation in the pathophysiology of UAP. Although activation of neutrophils, monocytes and lymphocytes has been shown in UAP, no studies have correlated the activation findings with clinical and angiographic features of patients with UAP.
Seventy-three patients undergoing coronary angiography were classified according to their ischaemic syndrome; stable angina pectoris (SAP) (n=25) and UAP (n=48). Patients with UAP were classified using the Braunwald classification; UAP class I (n=15), UAP class II (n=15), and UAP class III (n=18). Patients with UAP were also classified into a progression to myocardial infarction (MI(+)) group (n=15) and a non-progression to myocardial infarction (MI(-)) group (n=33). Venous blood samples were taken from all patients. Cell surface receptors (CD4, CD8, CD3, CD14, CD45, CD56+16, and HLA-DR) were detected by flow cytometry using monoclonal antibodies tagged with fluorescent markers and serum levels of C-reactive protein (CRP) were measured.
The serum levels of CRP and the percentages of HLA-DR, CD14, and CD16+56 were higher in UAP than SAP. The serum levels of CRP and percentages of HLA-DR, CD14, and CD16+56 were higher in UAP class II than UAP class I. The serum levels of CRP and percentages of HLA-DR, CD14, and CD16+56 were higher in UAP class III than UAP class II and UAP class I. The serum levels of CRP and percentages of CD16+56 were higher in the MI(+) group than the MI(-) group. The CRP levels in serum and the percentages of cell surface antigens had no correlation with extent of coronary artery disease (no differences among one, two or three vessels) but Type C lesion had significantly higher percentages of HLA-DR, CD14, CD16+56 and the serum levels of CRP than Type A and Type B lesions.
This investigation shows that inflammatory and immunologial components may be detectable in UAP and were correlated with the clinical severity, progression to myocardial infarction, and lesion morphology, but were not correlated with the extent of coronary artery disease.

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Evidence suggests that inflammation plays a key role in the pathogenesis of atherosclerosis. The chronic inflammatory process can develop to an acute clinical event by the induction of plaque rupture and therefore cause acute coronary syndromes.
The aim of this study was to determine the serum levels of the circulating acute-phase reactant C-reactive protein (CRP), which is a sensitive indicator of inflammation, in patients with chronic stable coronary artery disease (CAD) and acute coronary syndromes (ACS).
We studied 56 subjects: 1) 25 consecutive patients (18 men, 7 women; mean age, 68.5±14.3 years, range, 40-86) with unstable angina (UA) or acute myocardial infarction (AMI); 2) 31 consecutive patients (25 men, 6 women; mean age 64±12.7; range, 47-83, years) with signs and symptoms of clinically stable CAD. High-sensitivity-C-reactive protein (hs-CRP) levels were determined with a commercially available enzyme-linked immunoassay method.
In patients with unstable angina and AMI before reperfusion therapy, CRP levels were not significantly different to those in patients with stable CAD (5.96±2.26 versus 4.35±2.6 mg/L; P=0.12), but tended to be higher in patients with unstable angina and AMI. Baseline CRP levels in the subgroup of patients with AMI (6.49±2.28 mg/L) were significantly higher than levels in patients with stable CAD (4.35±2.6 mg/L; P=0.02).
CRP levels in patients with unstable angina and AMI were measured four times during a 72-hour period (0, 12, 24, and 72 hours). The lowest value was observed at baseline and differed significantly from values measured at any other time of the observation period (P<0.001; 5.96±2.26; 9.5±9.04, 18.25±11.02; 20.25±10.61). CRP levels after 12, 24, and 72 hours were also significantly different to the initial values for patients with stable CAD (P<0.01). There was no correlation between CRP and creatine kinase (CK), CK-MB isoenzyme, or troponin I positivity as markers for the extent of the myocardial injury during the observation period.
Baseline levels of serum CRP tended to be higher in patients with unstable angina or AMI but were not significantly different from levels in patients with chronic stable CAD. In the subgroup of patients with AMI, baseline CRP levels were significantly higher than the levels in patients with stable CAD. CRP as a marker of inflammation is significantly increased in patients with AMI and unstable angina shortly after the onset of symptoms (after a period of 12 hours), supporting the hypothesis of an activation of inflammatory mechanisms in patients with an acute coronary syndrome or AMI.

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The aim of the present study was to evaluate the tolerance to various exercises by determining the cardiovascular response to static and dynamic exercises in patients with nonvalvular atrial fibrillation.
Fifty patients (mean age: 63.6±10.3 years; male: 25, female: 25) with chronic (more than one year) nonvalvular atrial fibrillation were included in the study. All patients underwent exercise tests, adjusted appropriately according to their symptoms, as dynamic exercise on a Marquette Case 15 device according to a modified Bruce protocol. Heart rate, and systolic and diastolic arterial pressures were measured at rest and at all stages of the exercise; and the heart rate-pressure products were evaluated. A handgrip test was also conducted as static exercise. The measurements were made before, at the 1^st, 2^nd and 3^rd minutes, and in the recovery periods of the exercise.
The percent values of the changes of the 1^st, 2^nd and 3^rd minute measurements in relation to the initial values for both exercises were compared. In addition, the maximal responses to the exercise tests and the post exercise values were also compared. For statistical evaluations, the paired Student-t test was used.
Heart rate and pressure-heart rate product values obtained at 1, 2, and 3 minutes during the treadmill exercise test were significantly high compared to the handgrip values (P<0.0001). The arterial systolic and diastolic pressure values in the 1^st minute were also significantly higher during the handgrip test (P=0.0100 and P=0.0320, respectively). The values of diastolic arterial pressure at the 2^nd minute during the handgrip test, and systolic arterial pressure at the 3^rd minute during the treadmill test were found to be statistically significant (P=0.0240, P=0.0340, respectively). The mean exercise time and MET value during the treadmill exercise test were 7.18±2.65 minutes and 5.32±1.38 mL.kg^-1.dk^-1, respectively.
During the recovery period, the 5^th minute, heart rate and pressure-heart rate product values were significantly high after the treadmill test (P<0.0001).
In this study, we revealed that the heart rate response to static exercise was lower and the patients tolerated the static exercise better. Therefore, we decided that the short duration of static exercise is not harmful for the noncomplicated chronic atrial fibrillation cases.

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The aim of this study was to evaluate the safety and performance of the Autocapture pacing system during a 5-year follow-up period.
The study was conducted retrospectively between May 1996 and May 2001. Sixty consecutive patients who had undergone VVI pacemaker implantation using an Autocapture program with leads 1402T (n: 31) and 1452T (n: 29) were included in the study. Intraoperative measurements including a ventricular stimulation threshold test, sensing of intrinsic R wave (mV), and lead impedance (W) were done by a standard pacing system analyzer. Evoked responses (ER, mV) and polarization signals (PS, mV) were measured after the pocket was closed. Pacing thresholds by Autocapture (AC thrd, V) and Vario (Vario thrd, V), battery current (mA), and battery impedance (kW) were also repeated during predischarge and 1, 6, 12, 18, 24, 30, 40, 50, and 60 months after discharge. According to the ER and PS values an Autocapture algorithm could be activated in 49 patients (88%). The Autocapture algorithm remained active during the follow-up in all of these patients. In patients with inappropriate ER and PS values (11 patients, 12%), pacemakers were programmed to a VVIR pacing mode and Autocapture algorithm was inactivated. ER and PS values did not reach appropriate values to activate the Autocapture algorithm in any of these patients in consecutive follow-ups. Twenty-four-hour Holter monitoring could be conducted in 32 patients (53%). In all recordings, when the loss of capture occurred, it was confirmed that back-up pacing continued. When the first measurements recorded during implantation were compared to approximately the 5^th year measurements; ER (9.2 mV vs 9.6 mV), PS signal (1.13±0.30 mV vs 1.15±0.72 mV), AC thrd (0.4 V vs 1.2 V), Vario thrd (0.7 V vs 1.3 V), and lead impedance (502 ohm vs 620 ohm) were not changed significantly. Battery impedance increased 1 kOhm between 30-40 months of the implantation. Seven deaths occurred during follow-up. Three patients had fatal myocardial infarction, one died due to a non-cardiac event, and the remaining three died due to progressive heart failure. Conclusion: ER, R wave amplitude, and PS, which are the main parameters for the continuation of Autocapture function, did not change significantly during long-term follow-up. High output back up pacing provided additional safety for sudden rises in threshold. The Autocapture pacing algorithm was found to be effective and reliable during long-term follow-up.

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The clinical significance of induced nonclinical ventricular tachycardia (NCVT) in nonischemic dilated cardiomyopathy (DCM) remains controversial. Twenty-eight patients with sustained VT or ventricular fibrillation related to DCM underwent programmed ventricular stimulation (PVS) to induce VT. However, VT was not induced in four patients. Based on the morphology of induced ventricular arrhythmia, we classified the remaining 24 patients into NCVT (n=11) and clinical VT (CVT) groups (n=13), then evaluated the prognosis for a mean follow-up period of 22 months. The cycle length of induced NCVT was significantly shorter than that of induced CVT (277±38 ms vs 325±63 ms, P<0.05). Appropriate antiarrhythmic agents were selected by serial PVS in 36% of the NCVT group and in 38% of the CVT group (4/11 vs 5/13). Among patients who had been treated by PVS guided drug therapy, arrhythmic events were observed in 75% of the NCVT group and 80% of the CVT group (3/4 vs 4/5). The total incidence of sudden death in the NCVT group was higher than that in the CVT group (5/11: 45% vs 4/13: 31%). In conclusion, induced NCVT and CVT are refractory to pharmacological therapy and both have an important characteristic value in DCM.

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A germline mutation of the thyroid-stimulating hormone receptor (TSHR) gene has been reported to be associated with thyrotoxicosis and mitral valve prolapse syndrome (MVPS) in a Chinese family. The role of TSHR genetic variants in MVPS has not been well studied. This study investigated the possible relationship between the polymorphisms of codon 727 and 52 of the TSHR gene and MVPS among the Chinese population in Taiwan.
We studied 100 patients with MVPS diagnosed by echocardiography and 100 age- and sex-matched normal control subjects. The polymorphisms of codon 727 and 52 of the TSHR gene were identified by polymerase chain reaction-based restriction analysis.
There was no significant difference in either the genotype distribution or allelic frequencies between MVPS cases and controls for either TSHR gene D727E polymorphism (P=0.51 and 0.45, respectively ) or P52T polymorphism (P=0.60 and 0.31, respectively). The MVPS patients were divided into 2 subgroups: those with Graves' disease, and those without the thyroid disorder, and there were no statistical differences from the controls for both the TSHR gene D727E and P52T polymorphisms. Further categorization of the MVPS patients into mild and severe subgroups also revealed no statistical difference from controls for either the TSHR gene D727E or P52T polymorphisms.
These findings suggest that the codon 727 and 52 polymorphisms of the TSHR gene are not the suitable genetic markers of MVPS in Taiwan Chinese.

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Flow-mediated vasodilation (FMV), brachial artery flow (BAF), and brachial artery diameter were evaluated in 30 patients with congestive heart failure before and after cilazapril treatment.
While mean pulmonary artery pressure and pulmonary capillary wedge pressure decreased significantly, flow-mediated vasodilation and left ventricular ejection fraction increased significantly following cilazapril administration (P<0.001). Brachial artery diameter and brachial artery flow did not change following the treatment period (P>0.05).
In conclusion, short term cilazapril administration improved endothelial function and pulmonary pressure in patients with congestive heart failure.

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One of the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in the treatment of heart failure may derive from sympathoinhibition and the prevention of β-adrenergic desensitization. However, the roles of these properties in the overall effects of ACE inhibitor are not clear. We studied the effects of chronic enalapril treatment (20 mg/L in drinking water for 12 weeks) on left ventricular (LV) function, cardiac norepinephrine (NE), sympathetic neuronal function assessed by ¹³¹I-metaiodobenzylguanidine (MIBG), β-receptors, and isometric contraction of papillary muscle in rats with myocardial infarction (MI) induced by coronary artery ligation. Decreased LV function in the MI rats was associated with reduced cardiac NE content and MIBG uptake, and severely blunted responses of non-infarcted papillary muscle to isoproterenol, forskolin, and calcium. Enalapril attenuated LV remodeling in association with a reduction of the ventricular loading condition and restored baseline developed tension of non-infarcted papillary muscle to the level of sham-operated rats. However, enalapril did not improve cardiac NE content, MIBG uptake, or inotropic responsiveness to β-agonists. These results suggest that the major effect of the ACE inhibitor enalapril in the treatment of heart failure is not due to sympathoinhibition or restoration of β-adrenergic pathway in this model of heart failure.

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The aim of this study was to demonstrate that hypertrophied cardiac muscle is more sensitive to volume-overload than normal cardiac muscle. We assessed the mechanical function of isolated left ventricular papillary muscle from male spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY) submitted to volume overload caused by aortocaval fistula (ACF) for 30 days. Muscles were perfused with Krebs-Henseleit solution at 28°C and studied isometrically at a stimulation rate of 0.2 Hz. The ACF increased the right and left ventricular weight-to-body weight ratio in WKY rats; it also promoted right ventricular hypertrophy and further increased the basal hypertrophy in the left ventricle from SHR. The arterial systolic pressure was greater in SHR than in WKY rats, and decreased with ACF in both groups. Developed tension (DT) and maximum rate of DT (+dT/dt) were greater in the SHR-control than in the WKY-control (P<0.05); the time from peak tension to 50% relaxation (RT_1/2) was similar in these animals. ACF did not change any parameters in the SHR group and increased the resting tension in the WKY group. However, the significant difference observed between myocardial contraction performance in WKY-controls and SHR-controls disappeared when the SHR-ACF and WKY-controls were compared. Furthermore, RT_1/2 increased significantly in the SHR-ACF in relation to the WKY-controls. In conclusion, the data lead us to infer that volume-overload for 30 days promotes more mechanical functional changes in hypertrophied muscle than in normal cardiac muscle.

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The cardiovascular system is involved in 5% of the cases of Behcet's disease.Thrombophlebitis, aneurysm in arteries, pericarditis, myocarditis, valvular disease, ventricular arrhythmia, and conduction system disorders may occur. A case of Behcet's disease with complete proximal atrioventricular block is presented.

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