Prediction of readmissions and mortality in patients with heart failure: lessons from the IMPEDANCE-HF extended trial.

AIMS: Readmissions for heart failure (HF) are a major burden. We aimed to assess whether the extent of improvement in pulmonary fluid content (ΔPC) during HF hospitalization evaluated by lung impedance (LI), or indirectly by other clinical and laboratory parameters, predicts readmissions. METHODS AND RESULTS: The present study is based on pre-defined secondary analysis of the IMPEDANCE-HF extended trial comprising 266 HF patients at New York Heart Association Class II-IV and left ventricular ejection fraction ≤ 35% randomized to LI-guided or conventional therapy during long-term follow-up. Lung impedance-guided patients were followed for 58 ± 36 months and the control patients for 46 ± 34 months (P < 0.01) accounting for 253 and 478 HF hospitalizations, respectively (P < 0.01). Lung impedance, N-terminal pro-brain natriuretic peptide, weight, radiological score, New York Heart Association class, lung rales, leg oedema, or jugular venous pressure were measured at admission and discharge on each hospitalization in both groups with the difference defined as ΔPC. Average LI-assessed ΔPC was 12.1% vs. 9.2%, and time to HF readmission was 659 vs. 306 days in the LI-guided and control groups, respectively (P < 0.01). Lung impedance-based ΔPC predicted 30 and 90 day HF readmission better than ΔPC assessed by the other variables (P < 0.01). The readmission rate for HF was lower if ΔPC > median compared with ΔPC ≤ median for all parameters evaluated in both study groups with the most pronounced difference predicted by LI (P < 0.01). Net reclassification improvement analysis showed that adding LI to the traditional clinical and laboratory parameters improved the predictive power significantly. CONCLUSIONS: The extent of ΔPC improvement, primarily the LI based, during HF-hospitalization, and study group allocation strongly predicted readmission and event-free survival time.

Non-Invasive Lung IMPEDANCE-Guided Preemptive Treatment in Chronic Heart Failure Patients: A Randomized Controlled Trial (IMPEDANCE-HF Trial).

BACKGROUND: Previous investigations have suggested that lung impedance (LI)-guided treatment reduces hospitalizations for acute heart failure (AHF). A single-blind 2-center trial was performed to evaluate this hypothesis (ClinicalTrials.gov-NCT01315223). METHODS: The study population included 256 patients from 2 medical centers with chronic heart failure and left ventricular ejection fraction ≤35% in New York Heart Association class II-IV, who were admitted for AHF within 12 months before recruitment. Patients were randomized to a control group treated by clinical assessment and a monitored group whose therapy was also assisted by LI, and followed for at least 12 months. Noninvasive LI measurements were performed with a new high-sensitivity device. Patients, blinded to their assignment group, were scheduled for monthly visits in the outpatient clinics. The primary efficacy endpoint was AHF hospitalizations; the secondary endpoints were all-cause hospitalizations and mortality. RESULTS: There were 67 vs 158 AHF hospitalizations during the first year (P < .001) and 211 vs 386 AHF hospitalizations (P < .001) during the entire follow-up among the monitored patients (48 ± 32 months) and control patients (39 ± 26 months, P = .01), respectively. During the follow-up, there were 42 and 59 deaths (hazard ratio 0.52, 95% confidence interval 0.35-0.78, P = .002) with 13 and 31 of them resulting from heart failure (hazard ratio 0.30, 95% confidence interval 0.15-0.58 P < .001) in the monitored and control groups, respectively. The incidence of noncardiovascular death was similar. CONCLUSION: Our results seem to validate the concept that LI-guided preemptive treatment of chronic heart failure patients reduces hospitalizations for AHF as well as the incidence of heart failure, cardiovascular, and all-cause mortality.

[ISRAELI GUIDELINES FOR THE TREATMENT OF HYPERLIPIDEMIA - 2014 UPDATE].

Atherosclerosis is one of the leading causes of morbidity and mortality in the world, including in Israel. This document updates the clinical recommendations of the Israeli medical societies (The Society for Research, Prevention and Treatment of Atherosclerosis, The Israel Heart Society, The Israel Association of Family Physicians, The Israel Society of Internal Medicine) from 2012. The need for an update stems from new studies and from the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. These recommendations take into account the guidelines of leading medical organizations in the world, as well as the specific circumstances and needs of the medical system in Israel.

The Leaflex™ Catheter System - a viable treatment option alongside valve replacement? Preclinical feasibility of a novel device designed for fracturing aortic valve.

AIMS: To demonstrate the feasibility of the Leaflex™ Catheter System, a novel percutaneous device for fracturing valve calcification using mechanical impact in order to regain leaflet mobility. METHODS AND RESULTS: Radiographic analysis of calcium patterns in 90 ex vivo human aortic valve leaflets demonstrated that 82% of leaflets had a typical "bridge" or "half-bridge" pattern, which formed the basis for the catheter design. The therapeutic effect was quantified in 13 leaflets showing a reduction of 49±16% in leaflet resistance to folding after treatment. A pulsatile flow simulator was then used with 11 ex vivo valves demonstrating an increase in aortic valve area of 35±12%. Using gross pathology and histology on fresh calcified leaflets, we then verified that mechanical impacts do not entail excessive risk of embolisation. In vivo safety and usability were then confirmed in the ovine model. CONCLUSIONS: We demonstrated preclinically that it is feasible to improve valve function using the Leaflex™ technology. Once demonstrated clinically, such an approach may have an important role as preparation for or bridging to TAVI, as destination treatment for patients where TAVI is clinically or economically questionable and, in the future, maybe even as a means to slow disease progression in asymptomatic patients.

Derivation of baseline lung impedance in chronic heart failure patients: use for monitoring pulmonary congestion and predicting admissions for decompensation.

The instantaneous lung impedance (ILI) is one of the methods to assess pulmonary congestion or edema (PCE) in chronic heart failure (CHF) patients. Due to usually existing PCE in CHF patients when evaluated, baseline lung impedance (BLI) is unknown. Therefore, the relation of ILI to BLI is unknown. Our aim was to evaluate methods to calculate and appraise BLI or its derivative as reflecting the clinical status of CHF patients. ILI and New York Heart Association (NYHA) class were assessed in 222 patients (67 ± 11 years, LVEF <35 %) during 32 months of frequent outpatient clinic visits. ILI, measured in 120 asymptomatic patients at NYHA class I, with no congestion on the chest X-ray and a low-normal 6-min walk, was defined as BLI. Using measured BLI and ILI values in these patients, formulas for BLI calculation were derived based on logistic regression analysis or on the disparity between BLI and ILI values at different NYHA stages. Both models were equally reliable with <3 % difference between measured and calculated BLI (p = NS). ΔLIR = (ILI/BLI - 1) × 100 % reflected the degree of PCE, or deviation from baseline, correlated with NYHA class (r = -0.9, p < 0.001) and could serve for monitoring. Of study patients, 123 were re-hospitalized for PCE during follow up. Their ΔLIR decreased gradually from -21.7 ± 8.2 % 4 weeks pre-admission to -37.8 ± 9.3 % on admission (p < 0.001). Patients improved during hospital stay (NYHA 3.7 ± 0.5 to 2.9 ± 0.8, p < 0.0001) with ΔLIR increasing to -29.1 ± 12.0 % (p < 0.001). ΔLIR based on calculated BLI correlated with the clinical status of CHF patients and allowed the prediction of hospitalizations for PCE.

Relation of the systemic blood pressure to the collateral pressure distal to an infarct-related coronary artery occlusion during acute myocardial infarction.

Collaterals to occluded coronary arteries have been observed early after the onset of acute myocardial infarction (AMI). The pressure distal to the occluded segment of the culprit coronary artery (P(d)) is generated by collateral flow from the feeding coronary artery supplied by the systemic circulation. The aim of the study was to assess the relation between systemic blood pressure (BP) and P(d). Systemic BP and P(d) were measured simultaneously during intervention of totally occluded coronary arteries in 152 patients admitted for AMI. Patients were divided into groups by time from symptom onset to P(d) measurement. There was a significant positive correlation between P(d) and the systolic, diastolic, and mean BPs measured during the first 3 hours from symptom onset (n = 60; p <0.05, p <0.006, and p <0.005, respectively), from 3 to 12 hours (n = 56; p <0.02 for all), and >12 hours after symptom onset (n = 36; p <0.003 for all). The collateral flow, represented by calculated collateral flow index (mean 0.37 ± 0.14, median 0.36), was correlated with mean BP (p = 0.05) but not with diastolic or systolic BP (p = NS) in the overall study population. A direct relation was established during AMI between systemic BP and P(d) at all time intervals from symptom onset. Collateral flow index correlated with mean BP and was strongly associated with P(d) at all time intervals. In conclusion, the relation between P(d) and systemic BP suggests caution when administering therapy that may lower systemic BP during AMI before restoring flow in the occluded culprit artery, as it may compromise collateral pressure and exacerbate myocardial ischemia.

Relationship between the intensity of heparin anticoagulation and clinical outcomes in patients receiving glycoprotein IIb/IIIa inhibitors during primary percutaneous coronary intervention in acute myocardial infarction.

OBJECTIVES: We sought to determine the impact of the activated clotting time (ACT) in patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) with unfractionated heparin (UFH) and a glycoprotein IIb/IIIa inhibitor (GPI). BACKGROUND: UFH+GPI is commonly used during primary PCI for STEMI. UFH anticoagulation is titrated with ACT. METHODS: Patients randomized to UFH+GPI in HORIZONS-AMI who underwent primary PCI are included (N = 1,624). Initial UFH bolus was 60 IU kg(-1) (target ACT: 200-250 sec). Patients were divided into three tertiles of peak ACT (cutoffs 240 and 298 sec). The 30-day rates of major and minor bleeding, major adverse cardiovascular events (MACE), and net adverse clinical events (NACE; MACE or major bleeding) were determined. RESULTS: Mortality at 30 days occurred in 2.2, 3.3, and 3.5% of patients in the low to high ACT tertiles, respectively (P(trend) = 0.22). Nor was the peak ACT significantly related to major bleeding, MACE or NACE. However, minor bleeding was increased in the highest ACT tertile (14.7% vs. 14.2% vs. 19.4%, P(trend) = 0.04). By multivariable analysis peak ACT was not significantly related to major bleeding, mortality, MACE, and NACE but was a significant independent predictor of minor bleeding (odds ratio = 1.027 [1.013, 1.042], P < 0.001, for each 10 sec increase in ACT). CONCLUSIONS: In patients undergoing primary PCI for STEMI treated with UFH+GPI, the peak procedural ACT achieved does not have a substantial effect on major bleeding, mortality, or MACE, although lower peak ACT is associated with less minor bleeding.

Usefulness of lung impedance-guided pre-emptive therapy to prevent pulmonary edema during ST-elevation myocardial infarction and to improve long-term outcomes.

Patients sustaining an ST-segment elevation myocardial infarction (STEMI) frequently develop pulmonary congestion or pulmonary edema (PED). We previously showed that lung impedance (LI) threshold decrease of 12% to 14% from baseline during admission for STEMI marks the onset of the transition zone from interstitial to alveolar edema and predicts evolution to PED with 98% probability. The aim of this study was to prove that pre-emptive LI-guided treatment may prevent PED and improve clinical outcomes. Five hundred sixty patients with STEMI and no signs of heart failure underwent LI monitoring for 84 ± 36 hours. Maximal LI decrease throughout monitoring did not exceed 12% in 347 patients who did not develop PED (group 1). In 213 patients LI reached the threshold level and, although still asymptomatic (Killip class I), these patients were then randomized to conventional (group 2, n = 142) or LI-guided (group 3, n = 71) pre-emptive therapy. In group 3, treatment was initiated at randomization (LI = -13.8 ± 0.6%). In contrast, conventionally treated patients (group 2) were treated only at onset of dyspnea occurring 4.1 ± 3.1 hours after randomization (LI = -25.8 ± 4.3%, p <0.001). All patients in group 2 but only 8 patients in group 3 (11%) developed Killip class II to IV PED (p <0.001). Unadjusted hospital mortality, length of stay, 1-year readmission rate, 6-year mortality, and new-onset heart failure occurred less in group 3 (p <0.001). Multivariate analysis adjusted for age, left ventricular ejection fraction, risk factors, peak creatine kinase, and admission creatinine and hemoglobin levels showed improved clinical outcome in group 3 (p <0.001). In conclusion, LI-guided pre-emptive therapy in patients with STEMI decreases the incidence of in-hospital PED and results in better short- and long-term outcomes.

Novel acute collateral flow index in patients with total coronary artery occlusion during ST-elevation myocardial infarction.

BACKGROUND: The effect of collaterals to occluded coronary arteries during ST-elevation myocardial infarction (STEMI) is unclear. The conventional CVP-based formula to calculate collateral flow index during STEMI yields values higher than in elective patients, which prompted derivation of a modified formula, pertinent in STEMI when left ventricular mean diastolic pressure (LVMDP) is the extravascular pressure limiting collateral flow. We aimed to evaluate this new LVMDP-based acute collateral flow index (ACFI). METHODS AND RESULTS: The pressure distal to coronary artery occlusion (P(d)) was measured during intervention in 111 consecutive STEMI patients, 67 (61%) of whom underwent primary intervention, followed for 58 months. ACFI (0.18 ± 0.17, median 0.15) correlated with both P(d) and collateral grade (P<0.0001). Higher creatine kinase levels and white cell counts were measured in the lowest ACFI tertile compared with the highest tertile group (P<0.012). ACFI correlated slightly with early regional but not with global left ventricular ejection fraction or with long-term coronary events and mortality. CONCLUSIONS: The ACFI is appropriate for evaluating collateral function during STEMI. Collateral flow during STEMI may marginally limit myocardial damage but had no effect on left ventricular contraction or long-term mortality, most likely because of the low flow provided by emerging collaterals and the high proportion of patients undergoing intervention before the beneficial effect of collaterals could be realized.

A novel radiological score to assess lung fluid content during evolving acute heart failure in the course of acute myocardial infarction.

BACKGROUND: Monitoring of lung fluid content (LFC) in order to predict acute heart failure (AHF) during acute myocardial infarction (AMI) is an unmet challenge. AIM: To evaluate in AMI patients the ability of proposed radiological score (RS), which is the sum of selected radiological signs of congestion, to reflect correctly LFC, as assessed with repeat physical examinations and lung impedance (LI) measurements. METHODS: Chest X-rays were taken at baseline, when rales were detected, whenever indicated, and at conclusion of monitoring. RS grading for LFC assessment was: RS = 0-1 for normal X-ray, RS = 2-4 for interstitial congestion, and RS values of 5-6, 7-8 and 9-10 signified mild, moderate and severe alveolar edema, respectively. RESULTS: 624 AMI patients without AHF at baseline were monitored (94 ± 42 h). 476 patients (76%) with baseline RS of 0.3 ± 0.5 did not develop AHF. Overt AHF developed in 148 patients (24%) during monitoring; baseline RS (0.6 ± 0.8) reached 5.4 ± 0.7, 7.0 ± 0.8, and 9.8 ± 0.5 at the stages of mild, moderate, and severe alveolar edema, respectively. AHF resolved with treatment. RS decreased to 1.5 ± 1.3 (P < 0.01) and correlated with physical examination (r = 0.6, P < 0.01) and LI (r = -0.9, P < 0.01). CONCLUSION: RS correlated well with findings on physical examination during AHF and closely correlated with LI.

Collateral pressure and flow in acute myocardial infarction with total coronary occlusion correlate with angiographic collateral grade and creatine kinase levels.

BACKGROUND: The validity of angiographic collateral grade according to the Rentrop classification during acute myocardial infarction (AMI) and its relation to flow in occluded coronary arteries before angioplasty have never been evaluated. METHODS: We assessed the validity of the angiographic collateral grade according to Rentrop classification in relation to collateral pressure and flow beyond occluded coronary arteries during AMI. Pressure distal to coronary artery occlusions before balloon dilatation was measured in 111 patients undergoing angioplasty for AMI. We calculated the collateral flow index (CFI) and compared it to observed Rentrop grade and measured creatine kinase sum. RESULTS: The values of pressure distal to coronary artery occlusions with respect to collateral grades 0 to 3 were 33 +/- 12, 37 +/- 13, 42 +/- 10, and 60 +/- 14 mm Hg (P < .0001). Overall CFI was 0.35 +/- 0.13 (median 0.33), with CFI values of 0.3 +/- 0.13, 0.33 +/- 0.13, 0.39 +/- 0.1, and 0.57 +/- 0.2 for collateral grades 0 to 3, respectively (P < .0001). Larger creatine kinase elevation (P < .016) and higher white blood cell count (P < .022) were recorded in the lowest tertile CFI compared with highest tertile CFI group; but no difference in the global, regional, or infarct-related regional left ventricular contraction was found. CONCLUSIONS: These observations demonstrate that the Rentrop classification is valid in AMI patients with occluded coronary arteries and that collaterals are recruited acutely. These collaterals, whose pressure-derived CFI during AMI was shown for the first time to be higher than its value reported in chronic conditions, may limit the immediate myocardial damage or the systemic inflammatory response. No impact on global or regional cardiac contraction was detected in a population where most patients were treated early.

Pharmacodynamic effect and clinical efficacy of clopidogrel and prasugrel with or without a proton-pump inhibitor: an analysis of two randomised trials.

BACKGROUND: Proton-pump inhibitors (PPIs) are often prescribed in combination with thienopyridines. Conflicting data exist as to whether PPIs diminish the efficacy of clopidogrel. We assessed the association between PPI use, measures of platelet function, and clinical outcomes for patients treated with clopidogrel or prasugrel. METHODS: In the PRINCIPLE-TIMI 44 trial, the primary outcome was inhibition of platelet aggregation at 6 h assessed by light-transmission aggregometry. In the TRITON-TIMI 38 trial, the primary endpoint was the composite of cardiovascular death, myocardial infarction, or stroke. In both studies, PPI use was at physician's discretion. We used a multivariable Cox model with propensity score to assess the association of PPI use with clinical outcomes. FINDINGS: In the PRINCIPLE-TIMI 44 trial, 201 patients undergoing elective percutaneous coronary intervention were randomly assigned to prasugrel (n=102) or high-dose clopidogrel (n=99). Mean inhibition of platelet aggregation was significantly lower for patients on a PPI than for those not on a PPI at 6 h after a 600 mg clopidogrel loading dose (23.2+/-19.5% vs 35.2+/-20.9%, p=0.02), whereas a more modest difference was seen with and without a PPI after a 60 mg loading dose of prasugrel (69.6+/-13.5% vs 76.7+/-12.4%, p=0.054). In the TRITON-TIMI 38 trial, 13,608 patients with an acute coronary syndrome were randomly assigned to prasugrel (n=6813) or clopidogrel (n=6795). In this study, 33% (n=4529) of patients were on a PPI at randomisation. No association existed between PPI use and risk of the primary endpoint for patients treated with clopidogrel (adjusted hazard ratio [HR] 0.94, 95% CI 0.80-1.11) or prasugrel (1.00, 0.84-1.20). INTERPRETATION: The current findings do not support the need to avoid concomitant use of PPIs, when clinically indicated, in patients receiving clopidogrel or prasugrel. FUNDING: Daiichi Sankyo Company Limited and Eli Lilly and Company sponsored the trials. This analysis had no funding.

Effect of Metoprolol CR/XL on pulmonary artery pressure in chronic heart failure patients assessed by an implanted ultrasonic device with special emphasis on diurnal variation and exercise capacity.

OBJECTIVE: We evaluated the impact of Metoprolol CR/XL on the diurnal and exercise induced variation on Pulmonary Artery Pressure (PAP) in patients with Chronic Heart Failure (CHF) by implanted ultrasonic device. BACKGROUND: Metoprolol produces haemodynamic and clinical benefits in patients with chronic heart failure and improves survival rate. There is limited information about their effect on PAP, its diurnal and exercise induced variation in heart failure. This study evaluates the diurnal variation and effects of exercise capacity on PAP and impact of Metoprolol CR/XL (XL) on these variations on PAP in CHF patients. METHODS: In this first-in-man study, ten NYHA class III/IV patients were implanted with an ultrasonic pressure-monitoring device, followed a month later by loading with MXL 25 mg/day and uptitrated every two weeks to 200 mg/day. PAP was measured at each follow up. Diurnal variation was evaluated at baseline (no MXL), 100, and 200 mg/day MXL. Treadmill Test (TMT) was performed before and at each uptitration. Echocardiography was performed at one year. RESULTS: Uptitrating MXL caused a slight initial rise in PAP, followed by a subsequent decrease on reaching 200 mg/day dose. One patient showed repeated symptomatic rise in PAP indicating MXL intolerance and was discontinued from the uptitration. The nocturnal rise in PAP at baseline was reduced on reaching 200 mg/day MXL dose. Uptitrating MXL to 200mg7divide;day improved exercise time and metabolic equivalent tasks (METS) with no significant change in post TMT PAP. Ejection fraction also improved at one-year follow-up. CONCLUSIONS: PAP increases post exercise and diurnally in CHF patients. Slow and careful uptitration of MXL with simultaneous non-invasive monitoring of PAP may benefit in nocturnal rise and exercise capacity in CHF patients.

Impact of stent length on restenosis in patients with acute myocardial infarction treated with primary percutaneous coronary intervention: analysis based on data from the Trial to Assess the Use of the Cypher Stent in Acute Myocardial Infarction Treated with Balloon Angioplasty (TYPHOON).

AIMS: Stent length is a major predictor of restenosis in stable patients undergoing percutaneous coronary intervention (PCI) with bare metal stents (BMS). The effect of stent length is decreased by using drug eluting stents, however, this association had not been previously determined in patients with acute myocardial infarction (AMI). We sought to determine the impact of stent length on restenosis in patients who undergo primary PCI for AMI. METHODS AND RESULTS: Three-hundred and fifty-seven and 355 patients with AMI were included respectively in the BMS and SES (sirolimus eluting stents) arms of the Trial to Assess the Use of the Cypher Stent in Acute Myocardial Infarction Treated with Balloon Angioplasty (TYPHOON). Patients were divided into four subgroups based on the total length of the culprit lesion stented segment (in mm) : <18, >or=18 and <23, >or=23 and < 28, and >or=28 (groups 1 - 4 respectively). Target lesion revascularisation (TLR) and angiographic late loss were used to assess the restenotic process. Despite similar lesion length, average stent length was longer in patients treated with SES as compared to BMS 22.1+/-8.6 and 20.3+/-8.2 mm respectively, p=0.005. The rate of 12m death and AMI was similar in SES and BMS. There was no significance influence of stent length on % TLR neither in BMS (12.6, 10.1, 17.4 and 12.3 - subgroups 1-4 respectively) nor in SES (3.9, 5, 2.2 and 2.7 respectively). There was also no significant impact of stent length on angiographic late loss (mm) neither in BMS (0.7, 0.87, 0.84 and 0.92 respectively) nor in SES (0.32, 0.0, 0.11 and 0.3 respectively). CONCLUSIONS: Physicians tend to choose longer SES than BMS for a similar lesion length during primary PCI for AMI. Interestingly, stent length did not affect clinical or angiographic restenosis neither in BMS nor in SES in this group of patients who underwent primary PCI for acute MI. This data challenges current practice concerning the chosen stent length in patients with AMI.

Apical thrombus associated with Takotsubo cardiomyopathy in a young woman.

We report a case of Takotsubo cardiomyopathy complicated by left ventricular apical thrombus in a young woman; the thrombus and wall motion abnormalities disappeared after 3 weeks of anticoagulant therapy. These findings suggest that appropriate anticoagulation therapy should be performed in patients with Takotsubo cardiomyopathy until wall motion abnormalities improve.

Wireless acoustic communication with a miniature pressure sensor in the pulmonary artery for disease surveillance and therapy of patients with congestive heart failure.

OBJECTIVES: The purpose of this study was to examine the feasibility of repeated pulmonary artery (PA) pressure determinations using a newly developed acoustic wireless implanted communication system. BACKGROUND: Congestive heart failure management strategies based on monitored intracardiac hemodynamics in patients receiving the best-available therapy may improve outcome. Although electromagnetic communication requires a large antenna for sufficient energy transfer, acoustic energy readily penetrates deep into the body, uses little energy, and uses small internal transducers for bidirectional operation. METHODS: A miniature device was developed and implanted using right heart catheterization. The ability to obtain PA pressure from the implant using wireless acoustic communication was examined in 8 pigs and 10 patients with congestive heart failure. Macroscopic and histopathologic examinations were performed at 6 months after implantation. The accuracy of PA pressure measurement was determined by comparison with simultaneous pressures from a Millar catheter. RESULTS: The device was successfully implanted in the PA using right heart catheterization. There were no implantation or later device-related complications. Pulmonary artery pressure tracings were repeatedly obtained from all implants. Normal reactions to intravascular implant were observed macroscopically and in histologic sections. Standard deviations of the difference between implant and Millar PA diastolic pressure were 1.45 and 1.2 mm Hg (animals and humans, respectively). Data were useful for patient management. CONCLUSIONS: This pilot study demonstrates, for the first time, that acoustic wireless communication with a miniature implanted sensor is feasible and provides repeated PA pressure measurement. This feat makes possible multiple novel applications for monitoring and therapeutic interventions based on measurements from deeply implanted devices.