Enabling electromechanical transduction in silicon nanowire mechanical resonators fabricated by focused ion beam implantation.

We present the fabrication of silicon nanowire (SiNW) mechanical resonators by a resistless process based on focused ion beam local gallium implantation, selective silicon etching and diffusive boron doping. Suspended, doubly clamped SiNWs fabricated by this process presents a good electrical conductivity which enables the electrical read-out of the SiNW oscillation. During the fabrication process, gallium implantation induces the amorphization of silicon that, together with the incorporation of gallium into the irradiated volume, increases the electrical resistivity to values higher than 3 Ω m, resulting in an unacceptably high resistance for electrical transduction. We show that the conductivity of the SiNWs can be restored by performing a high temperature doping process, which allows us to recover the crystalline structure of the silicon and to achieve a controlled resistivity of the structures. Raman spectroscopy and TEM microscopy are used to characterize the recovery of crystallinity, while electrical measurements show a resistivity of 10(-4) Ω m. This resistivity allows to obtain excellent electromechanical transduction, which is employed to characterize the high frequency mechanical response by electrical methods.

Horizontally patterned Si nanowire growth for nanomechanical devices.

We report a method to pattern horizontal vapor-liquid-solid growth of Si nanowires at vertical sidewalls of Si microstructures. The method allows one to produce either single nanowire structures or well-ordered nanowire arrays with predefined growth positions, thus enabling a practical development of nanomechanical devices that exploit the singular properties of Si nanowires. In particular, we demonstrate the fabrication of doubly clamped nanowire resonators and resonator arrays whose mechanical resonances can be measured by optical or electrical readout. We also show that the fabrication method enables the electrical readout of the resonant mode splitting of nanowire resonators in the VHF range, which allows the application of such an effect for enhanced nanomechanical sensing with nanowire resonators.

Metal microelectromechanical oscillator exhibiting ultra-high water vapor resolution.

Water vapor sensing characterization of a metal resonator fabricated with an industrial 0.35 µm CMOS technology is reported. The resonator frequency is ∼13.2 MHz and exhibits a sensitivity magnitude of ∼3.5 kHz per %RH without requiring any additional hygroscopic coating layer. An on-chip integrated oscillator circuit enables an unprecedented resolution of 0.005 %RH.

Left main coronary artery atresia: literature review and therapeutical considerations.

OBJECTIVE: Left main coronary artery atresia is a rare coronary anomaly in which there is no left coronary ostium, the proximal left main trunk ends blindly, blood flows from the right coronary artery to the left via small collateral arteries and retrogradely in at least one of the left-sided arteries. Since published case reports are few and rather scattered, no comprehensive information about this uncommon anomaly is available. METHODS: A through search for published cases of left main coronary atresia was performed in the major medical journals by electronic (MEDLINE and INTERNET) and hand-scanning. RESULTS: The authors found 28 cases of left main atresia (including two from their own experience), 15 of which were pediatric; five of these cases had associated cardiac anomalies. While pediatric patients were usually overtly symptomatic early in their life (syncope, dyspnea, sudden death, failure to thrive, infarction, ventricular tachycardia), adult patients began showing symptoms (angina, dyspnea, sudden death) only at an advanced age; associated coronary atherosclerosis seemed to be uncommon, though (2/13 adult patients, 15%). We know of only one asymptomatic patient, a 76-year old lady who had died of unrelated causes; in her case left main atresia was an unforeseen autopsy finding. Four untreated patients had died suddenly; most of the others were highly symptomatic and required surgical therapy, usually as direct coronary artery revascularization via one or more saphenous vein or mammary artery grafts to the left-sided arteries; all revascularized patients were reported to be alive and well; in one pediatric case the left main coronary artery was reconstructed using an aortic wall baffle, with a good result. In contrast, the outcome of patients who did not receive revascularization has been poor. CONCLUSION: In light of the favorable results obtained by surgical therapy, the authors endorse prompt coronary artery revascularization for all patients with left main coronary artery atresia.

[Short and intermediate term clinical outcome in patients with cardiogenic shock treated with aortic counterpulsation]. / Evoluzione clinica a breve e medio termine di pazienti cardiopatici in shock cardiogeno trattati con contropulsazione aortica.

BACKGROUND: Despite improvements in coronary care, cardiogenic shock (CS) remains the leading cause of death in patients with dramatic cardiac diseases of which acute myocardial infarction (AMI) is the most frequent event. Conventional therapy for CS with coronary care unit (CCU) monitoring and vasopressor agents to support blood pressure has historically been associated with an 80% to 90% mortality rate in large series. Intra-aortic balloon pump (IABP) therapy for shock results in initial favourable clinical and haemodynamic responses, but ultimately, in most patients, death is merely delayed and hospital mortality still exceeds 80%. In several recent non-randomised series, coronary revascularisation performed early in the course of CS with the use of coronary artery by-pass grafting (CABG) or coronary angioplasty (PTCA) resulted in an apparent reduction in the hospital mortality rate to less than 50% in selected patients with shock. OBJECTIVES: This study reviews our experience of cardiogenic shock treatment at a time when standard care included aggressive use of the intra-aortic balloon pump counterpulsation, cardiac catheterisation, coronary angioplasty and/or coronary artery by-pass grafting, ventricular septal defect and mitral incompetence repair. METHODS: We retrospectively analysed 20 patients (13 M and 7 F, with an average age of 62 years and a half) affected by cardiogenic shock consecutively admitted to our CCU between October 1, 1992 and April 1, 1995. Fifteen patients (pts) were hospitalised for AMI, shock and pump failure (2 of them with pulmonary oedema), all with admittance delay less than 24 hours. Five patients were hospitalised for AMI with shock and mechanical defects, of which 3 pts with AMI and ventricular septal rupture and 2 pts with AMI and mitral regurgitation. All patients underwent IABP, coronary angiography (CA) and then were treated with PTCA, CABG and cardiac surgery or medical treatment. RESULTS: On the whole, 7 pts died (35%): 4 of shock, 1 of haemorrhagic complications, 1 of septic shock in the CCU, and 1 of heart failure after CABG in cardiosurgery. One more patient died of heart failure two months after discharge (late mortality 5%). Out of the 15 patients hospitalised with AMI, shock and pump failure, 13 patients with AMI and CS less than 24 hrs were treated as follows: 1 patient was successfully submitted to emergency CABG and 12 patients to PTCA of the infarct related artery (IRA). Eight patients enjoyed a good outcome, but 1 patient died of haemorrhagic complications and 4 with a persistently occluded IRA also died (3 in the CCU and 1 after CABG). Of the 2 remaining pts with AMI, shock and pulmonary oedema, 1 patient underwent CABG with success and 1 patient with the 3-vessel disease was submitted to PTCA with reperfusion of the IRA, but he died from reocclusion three days later. Out of the 5 patients with AMI, shock and mechanical defects, 3 patients with AMI and septal ventricular rupture underwent cardiac surgery and CABG with early and late success. One of the 2 patients with AMI, shock and mitral regurgitation underwent cardiac surgery with valve repair and CABG and had a good outcome, the other died from septic complications in the CCU. CONCLUSIONS: IABP is an useful device for stabilising patients in cardiogenic shock and safely performing angiography as well as PTCA, CABG or surgical correction of all mechanical complications with a more stable haemodynamic balance. Therefore, IABP is an useful tool to improve successful coronary revascularisation after direct PTCA or direct CABG. These data also suggest that the combination of successful coronary revascularisation and intra-aortic balloon pumping can improve survival in pts with cardiogenic shock complicating AMI with early pump failure.

[The recurrence of pulmonary embolism during heparin therapy after thrombolysis in the acute phase: a clinical case report]. / Recidiva di embolia polmonare in corso di terapia eparinica dopo trombolisi in fase acuta: descrizione di un caso clinico.

We report a case of a 61-year-old woman admitted to our Coronary Care Unit for pulmonary embolism following cholecystectomy. After thrombolytic therapy, and during treatment with heparin (administered as a continuous intravenous infusion in the standard dose), the patient had a recurrence of pulmonary embolism and a subsequent implant of a Gianturco-Rohem vena cava filter. The patient presented an initial reduction in the number of platelets from 477 x 10(3)/microliters to 360 x 10(3)/microliters that was ascribed to a heparin side effect or to a blocking of the platelets in a massive pulmonary thrombosis. A predischarge platelet count, however, showed an elevated number of thrombocytes (944 x 10(3)/microliters) and hyperfibrinogenemia (fibrinogen = 750 mg/dl). Essential thrombocythemia was demonstrated and treated with interferon alpha-2b-recombinant 3,000,000 U.I. on alternate days with a reduction in platelets to 450 x 10(3)/microliters. This case demonstrates the necessity of exploring, during pulmonary embolism, all possible causes of hypercoagulability in the course of thrombolytic therapy.

Effects of urokinase and heparin on minimal cross-sectional area of the culprit narrowing in unstable angina pectoris.

The immediate and delayed effects of urokinase and heparin on minimal cross-sectional area of a patent ischemia-producing coronary artery were prospectively investigated in 43 patients with unstable angina. After baseline angiography, patients were randomized to 3 different treatment groups: group I--urokinase (1,000,000 U intravenous bolus dose), followed by heparin infusion 3 hours later; group II--heparin (10,000 U intravenous bolus, followed by continuous infusion); and group III--conventional therapy only (intravenous nitroglycerin, beta blockers and calcium antagonists). Angiography was repeated at 1 hour and at 8 days of treatment and minimal cross-sectional area was determined in the 35 patients who completed the study. In group I, minimal cross-sectional area increased from 0.84 +/- 0.48 mm2 at baseline to 0.94 +/- 0.49 mm2 at 1 hour (p less than 0.05), and to 1.00 +/- 0.51 mm2 at 8 days (p less than 0.01 vs baseline). In group II, a significant increase in minimal cross-sectional area was observed only at the 8-day angiography (0.64 +/- 0.39 mm2 at baseline; 0.67 +/- 0.37 mm2 at 1 hour [p = not significant]; and 0.79 +/- 0.48 mm2 at 8 days [p less than 0.01] vs baseline). In group III, no significant changes in minimal cross-sectional area occurred either at 1 hour or at 8 days. Thus, both urokinase and heparin improved lesion geometry in patients with unstable angina, although a large individual variation was noticed. The effect occurred earlier with urokinase than with heparin.

Angiographic morphology and response to therapy in unstable angina.

The coronary anatomy of 69 patients with unstable angina, subgrouped according to response to medical therapy, was investigated. All patients received oral treatment with nitrates, calcium antagonists, and beta-blocking agents. When combined oral treatment was not effective, an intravenous infusion of nitrates (10-100 micrograms/min) was subsequently administered. Coronary arteriography was performed within hours (14 +/- 9 h) from the last episode of chest pain in 28 patients refractory to medical treatment, while in 41 patients who became asymptomatic during medical therapy, angiography was performed after an observation period of several days (8 +/- 6 days). On angiography, the nonresponder group was characterized by a prevalence of eccentric and multiple lesions, and by a 46% incidence of thrombi (p less than 0.001). Recurrent symptoms requiring emergency bypass operation were common in this group. In patients responsive to medical treatment, a high percentage of concentric lesions (37%) and totally occluded (34%) coronary arteries was found (p less than 0.05). No infarcts and low rate of recurrent angina were noted in these patients during hospitalization. In conclusion, the finding of intracoronary thrombotic material and eccentric or multiple lesions can be an accurate markers of the active phase of the disease, while "silent" occlusion of the involved vessel may be accompanied by relief of symptoms during medical therapy.

Clinical experience with urokinase in intracoronary thrombolysis.

A prospective nonrandomized study of the thrombolytic efficacy and dose-response effect of a high-molecular-weight urokinase, administered into the coronary artery, was conducted in 63 patients with acute myocardial infarction. Urokinase was infused (up to 180 min) at rates of 2000, 4000, 6000, and 10,000 IU/min in four consecutive groups of patients within 184 +/- 70 min following onset of chest pain. Of 54 patients with complete occlusion of the infarct-related vessel, 48 (89%) exhibited complete reperfusion. In 9 patients with incomplete occlusion, the degree of coronary stenosis was reduced with concomitant improvement in antegrade flow. The median effective dosage requirement of urokinase to reperfuse 50% of the treated patients was 180,000 IU. A relationship between the four infusion regimens and successful reperfusion was not found. The time to reperfusion, however, ranging from 42 +/- 30 to 60 +/- 41 min, appeared to be dose dependent. The reocclusion rate at follow-up (10-14 days) was 18%. Ejection fraction improved (40 +/- 8 vs. 47 +/- 8%, p = 0.002) in patients with low pretreatment values and in those treated within 2 h of the onset of symptoms. In-hospital mortality was 9%. Hemorrhage requiring transfusion occurred in 8% of the patients. None of the patients had levels of circulating fibrinogen inferior to 100 mg/dl. We conclude that urokinase can induce timely coronary reperfusion in patients with evolving myocardial infarction, at moderate infusion rates, and with concomitant induction of an only mild systemic lytic state.

[Ventricular repolarization abnormalities and arrhythmia in the athlete. A long-term follow-up clinical case]. / Anomalie della ripolarizzazione ventricolare e aritmie nell'atleta. Caso clinico di osservazione prolungata.

Clinical and prognostic significance of ventricular repolarization anomalies in sportsmen is still uncertain, even if they are most commonly regarded as benign. We studied a patient in whom those manifestations didn't show any progression within 30 years even after interruption of athletics and were related to idiopathic hypertrophic cardiomyopathy. Anatomical findings were combined with cardiac rhythm and conduction disturbances (paroxysmal atrial flutter, premature contractions, 2nd degree AV block). In our patient ventricular repolarization anomalies, even though without a negative prognosis, can't be related to "athlete's heart" but rather to organic cardiomyopathy.

Efficacy of intracoronary and intravenous urokinase in acute myocardial infarction.

The efficacy of intracoronary and intravenous urokinase was studied in 83 patients with acute evolving myocardial infarction. Urokinase was administered intracoronary in 48 patients with a success rate of 89% obtained after 47 +/- 32 minutes of infusion of a dose of 255.000 +/- 224.000 IU. In-hospital mortality in this group of patients was 10%. Severe arrhythmias were observed in 33% of the patients and the reocclusion rate at the re-study was 16%. Intravenous urokinase was administered as 200.000 IU bolus followed by 1.220.000 IU infusion in 21 patients. Angiography performed in this group of patients 48 hours after therapy showed a patency rate of 66%. A single intravenous bolus of 500.000 IU of urokinase was administered to 14 patients. At angiography all patients but one were found reperfused. The value of intravenous low-dose bolus injection of urokinase in acute myocardial infarction needs hower to be assessed with a properly designed clinical trial.

[Intracoronary thrombolysis]. / Trombolisi intracoronarica.

Intracoronary Urokinase administration was attempted in 42 patients with acute myocardial infarction. One patient died before Urokinase infusion could be started, two patients during treatment. 34 patients (83%) had total occlusion of a coronary vessel, 7 patients (17%) had a subtotal occlusion. Urokinase was administered at a rate of 10.000 IU/min in 11 consecutive patients (Group I), 6000 IU/min in 11 patients (Group II), 4000 IU/min in 11 patients (Group III), 2000 IU/min in 8 patients (Group IV). Recanalization of the occluded vessel or amelioration of the subocclusion was obtained in 36 patients (88%). 35 patients were controlled 12 days after the procedure, with coronary-angiography and left ventriculography. Patency persisted in 31 patients and successful thrombolysis was associated with significant improvement of left ventricular ejection fraction in those patients with depressed ventricular function before Urokinase treatment.

Intracoronary thrombolysis with urokinase in acute myocardial infarction. Effects on reperfusion and left ventricular wall motion.

Intracoronary Urokinase administration was attempted in 20 patients (mean age 56 years) during the early phase of an acute evolving myocardial infarction. One patient died before urokinase infusion could be started. Out of the remaining nineteen patients, eighteen had total occlusion of a coronary vessel; one patient, in cardiogenic shock, failed to show occluding thrombi of the vessel related to the ECG site of infarction, and died during the procedure. Urokinase was administered at a rate of 4000 IU/min in 7 consecutive patients (Group I), 6000 IU/min in 5 patients (Group II), and 10000 IU/min in 6 patients (Group III). Recanalization of the occluded vessel was obtained in 16 patients (88%). The reperfusion time was 52 +/- 33 min. No significant variation in reperfusion time was noted in the three groups of patients treated. The time elapsed between the onset of symptoms and the successful recanalization was in our patients 4.3 +/- 1.8 hours. Ventricular arrhythmias, which required treatment, appeared after reperfusion in five patients. No serious hemorrhagic complications were noted. In fourteen patients ventriculography was performed before and immediately after thrombolysis: 15 patients had the study repeated 12 days after the procedure. Patency persisted in 13 patients and successful thrombolysis was associated with significant improvement in left ventricular ejection fraction and segmental wall motion. Our data demonstrate that different doses of Urokinase can be safely and successfully used to produce intracoronary thrombolysis in the majority of patients with acute myocardial infarction.

Papillary muscle necrosis in a neonatal autopsy population: incidence and associated clinical manifestations.

Papillary muscle necrosis was found in 24 of 84 neonates without congenital heart disease who died and were autopsied during a 17-month study period. The lesion was most prevalent in infants greater than or equal to 3,000 gm birth weight (59%), but papillary muscle necrosis was also noted in 25% of the infants of medium birth weight (1,500 to 2,999 gm) and in 19% of the very low-birth-weight infants (less than 1,500 gm). Papillary muscle necrosis in the highest birth-weight group correlated with five-minute Apgar scores of 6 or less, meconium aspiration syndrome, seizures, congestive heart failure, increased cardiothoracic ratio (greater than or equal to 0.60), and ischemic changes on electrocardiogram. In the medium- and very low-birth-weight groups, however, patients with papillary muscle necrosis could seldom be differentiated clinically from their birth-weight peers without the lesion, even in retrospect.

Recognition of developing left ventricular outflow tract obstruction in complete transposition of the great arteries.

In the months following balloon atrial septostomy for complete transposition of the great arteries (TGA), clinical deterioration is often ascribed to closure of the septostomy. Of 16 neonates with TGA, 5 showed early clinical deterioration. Each had an adequate septostomy at operation. Deterioration was characterized clinically by increasing cyanosis and radiographically by progressive diminution in pulmonary vascularity. Subsequent catheterization and axial cineangiography demonstrated that pulmonary flow had decreased, probably secondary to a progressive form of left ventricular outflow tract obstruction (LVOTO) characterized by bulging of the ventricular septum with mitral valve apposition. It is important to recognize this phenomenon as an aid in predicting which children will need early surgical intervention.

Left ventricular outflow tract obstruction in transposition of the great arteries: an angiographic study of 74 cases.

Recent advances in techniques of angiocardiography now allow highly accurate assessment of the anatomy of the left ventricle in patients with transposition of the great arteries. The cineangiograms of 225 children with transposition were reviewed using axial cineangiographic techniques and 33 percent were found to have significant left ventricular outflow tract obstruction with or without coexisting ventricular septal defects. The varieties of left ventricular outflow tract obstruction and the associated ventricular septal defects found in this group of patients are described, illustrated and correlated. The advantages of axial angiocardiography in the diagnosis of transposition are pointed out, and the techniques used to produce the axial angiocardiograms are reviewed.