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Objectives: The purpose of this study was to determine if combined intense lifestyle and pharmacologic lipid treatment reduce myocardial perfusion abnormalities and coronary events in comparison to usual-care cholesterol-lowering drugs and whether perfusion changes predict outcomes.Background: Lifestyle and lipid drugs separately benefit patients with coronary artery disease (CAD).Methods: A total of 409 patients with CAD, who underwent myocardial perfusion imaging by dipyridamole positron emission tomography at baseline and after 2.6 years, had quantitative size/severity of perfusion defects measured objectively by automated software with follow-up for five additional years for coronary artery bypass graft, percutaneous coronary intervention, myocardial infarction, or cardiac death. Patients were categorized blindly according to prospective, predefined criteria as "poor" treatment without diet or lipid drugs, or smoking; "moderate" treatment on American Heart Association diet and lipid-lowering drugs or on strict low-fat diet (<10% of calories) without lipid drugs; and "maximal" treatment with diet <10% of calories as fat, regular exercise, and lipid active drugs dosed to target goals of low-density lipoproteins <2.3 mmol/l (90 mg/dl), high-density lipoproteins >1.2 mmol/l (45 mg/dl), and triglycerides <1.1 mmol/l (100 mg/dl).Results: Over five years, coronary events occurred in 6.6%, 20.3%, and 30.6% of patients on maximal, moderate, and poor treatment, respectively (p = 0.001). Size/severity of perfusion abnormalities significantly decreased for patients receiving maximal treatment and increased for patients undergoing moderate and poor treatment (p = 0.003 and 0.0001, respectively). Combined intense lifestyle change plus lipid active drugs and severity/change of perfusion abnormalities independently predicted cardiac events.Conclusions: Intense lifestyle and pharmacologic lipid treatment reduce size/severity of myocardial perfusion abnormalities and cardiac events compared with usual-care cholesterol-lowering drugs. Perfusion changes parallel treatment intensity and predict outcomes. [ABSTRACT FROM AUTHOR]

Background: Subendocardial ischemia is commonly diagnosed but not quantified by imaging., Objectives: This study sought to define size and severity of subendocardial and transmural stress perfusion deficits, clinical associations, and outcomes., Methods: Regional rest-stress perfusion in mL/min/g, coronary flow reserve, coronary flow capacity (CFC), relative stress flow, subendocardial stress-to-rest ratio and stress subendocardial-to-subepicardial ratio as percentage of left ventricle were measured by positron emission tomography (PET) with rubidium Rb 82 and dipyridamole stress in serial 6,331 diagnostic PETs with prospective 10-year follow-up for major adverse cardiac events with and without revascularization., Results: Of 6,331 diagnostic PETs, 1,316 (20.7%) had severely reduced CFC with 41.4% having angina or ST-segment depression (STΔ) >1 mm during hyperemic stress, increasing with size. For 5,015 PETs with no severe CFC abnormality, 402 (8%) had angina or STΔ during stress, and 82% had abnormal subendocardial perfusion with 8.7% having angina or STΔ >1 mm during dipyridamole stress. Of 947 cases with stress-induced angina or STΔ >1 mm, 945 (99.8%) had reduced transmural or subendocardial perfusion reflecting sufficient microvascular function to increase coronary blood flow and reduce intracoronary pressure, causing reduced subendocardial perfusion; only 2 (0.2%) had normal subendocardial perfusion, suggesting microvascular disease as the cause of the angina. Over 10-year follow-up (mean 5 years), severely reduced CFC associated with major adverse cardiac events of 44.4% compared to 8.8% for no severe CFC (unadjusted P < 0.00001) and mortality of 15.2% without and 6.9% with revascularization (P < 0.00002) confirmed by multivariable Cox regression modeling. For no severe CFC, mortality was 3% with and without revascularization (P = 0.90)., Conclusions: Reduced subendocardial perfusion on dipyridamole PET without regional stress perfusion defects is common without angina, has low risk of major adverse cardiac events, reflecting asymptomatic nonobstructive diffuse coronary artery disease, or angina without stenosis. Severely reduced CFC causes angina in fewer than one-half of cases but incurs high mortality risk that is significantly reduced after revascularization., Competing Interests: Funding Support and Author Disclosures Research supported by internal funds of the Weatherhead PET Center. Dr Gould has received internal funding from the Weatherhead PET Center and is the applicant for 510(k) U.S. Food and Drug Administration–cleared HeartSee K202679 PET software. Dr Johnson has received internal funding from Weatherhead PET Center for Preventing and Reversing Atherosclerosis and research support from St. Jude Medical (for CONTRAST [Can Contrast Injection Better Approximate FFR Compared to Pure Resting Physiology] trial; NCT02184117) and Volcano/Philips Corporation (for the DEFINE-FLOW [Combined Pressure and Flow Measurements to Guide Treatment of Coronary Stenoses] trial; NCT02328820). To avoid any conflict of interest, Drs Gould, Nguyen, Johnson, and Kirkeeide waived their rights to the royalties that they were personally eligible to receive from sales of the intellectual property developed by them and licensed by the University of Texas Health Science Center (UTHealth) to third parties. UTHealth approved their request that all derived royalties be redirected to student scholarships or UTHealth’s Weatherhead PET Center research. UTHealth has a financial interest related to intellectual property via its affiliation with the UTHealth’s Weatherhead PET Imaging Center. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Because randomized coronary revascularization trials in stable coronary artery disease (CAD) have shown no reduced myocardial infarction (MI) or mortality, the threshold of quantitative myocardial perfusion severity was analyzed for association with reduced death, MI, or stroke after revascularization within 90 d after PET. Methods: In a prospective long-term cohort of stable CAD, regional, artery-specific, quantitative myocardial perfusion by PET, coronary revascularization within 90 d after PET, and all-cause death, MI, and stroke (DMS) at 9-y follow-up (mean ± SD, 3.0 ± 2.3 y) were analyzed by multivariate Cox regression models and propensity analysis. Results: For 3,774 sequential rest-stress PET scans, regional, artery-specific, severely reduced coronary flow capacity (CFC) (coronary flow reserve ≤ 1.27 and stress perfusion ≤ 0.83 cc/min/g) associated with 60% increased hazard ratio for major adverse cardiovascular events and 30% increased hazard of DMS that was significantly reduced by 54% associated with revascularization within 90 d after PET ( P = 0.0369), compared with moderate or mild CFC, coronary flow reserve, other PET metrics or medical treatment alone. Depending on severity threshold for statistical certainty, up to 19% of this clinical cohort had CFC severity associated with reduced DMS after revascularization. Conclusion: CFC by PET provides objective, regional, artery-specific, size-severity physiologic quantification of CAD severity associated with high risk of DMS that is significantly reduced after revascularization within 90 d after PET, an association not seen for moderate to mild perfusion abnormalities or medical treatment alone., (© 2019 by the Society of Nuclear Medicine and Molecular Imaging.)

In 1987 and 1990 in Massachusetts, surveys were conducted to determine the size, pattern of distribution, and trends in the population of children assisted by medical technology. The authors obtained an unduplicated count of all Massachusetts children from 3 months to 18 years of age who used one or more of the following: tracheostomy, respirator, oxygen, suctioning, gastrostomy, jejunal or nasogastric feedings, ostomies, urethral catheterization, ureteral diversion, intravenous access, or dialysis. By comparing counts obtained from medical and educational sources, the authors were able to perform a capture-recapture analysis to estimate the overall number of children dependent upon these technologies. The number of children identified in our surveys increased from 1,085 in 1987 to 1,540 in 1990. However, the capture-recapture analysis yielded estimates of 2,147 plus or minus 230 for 1987 and 2,237 plus or minus 131 for 1990. This suggests that the population of children dependent upon medical technology was essentially stable during this period, and that the 42 percent increase in the number of children identified in our survey reflected improved sampling techniques. During the 3 years, shifts in the pattern of technology use were noted, however. Use of oxygen and gastrostomy increased, and urostomy use declined. A change in the age distribution of the children was also documented, with a shift in the preponderence of technology use from 12 to 24 months in 1987 to children in the first year of life in 1990. Using the 1990 estimate and the 1990 U.S. census figures, an overall prevalence estimate of 0.16 percent was calculated. Applying this to the U.S.child population yields an estimate of 101,800 children assisted by medical technology nationwide(assuming comparable technology use in other States). This information will facilitate policy analysis and program planning on regional and national levels for this medically complex group of children.

The increasing number of children assisted by medical technology in the U.S. has led to a need for systematic planning for the children's care in community settings such as schools. Project School Care in Massachusetts provides consultation to school systems as schools respond to the challenge of integrating children assisted by medical technology into educational settings. The model of practice described includes the step-wise planning process and the ensuing training, enrollment, and monitoring procedures. Implications are explored with particular emphasis on upgrading of skills at all medical and educational levels. More input from school health personnel in administrative decision-making around enrollment of children with special health care needs is recommended. For these children, a health care plan should be incorporated into their Individualized Education Plans and into their school records.

Potassium loss from damaged myocardial cells is linearly related to CPK enzyme loss reflecting extent of necrosis. The potassium analog, rubidium-82 (82Rb), is extracted after i.v. injection and retained in viable myocardium but is not trapped or washed out of necrotic regions. To compare myocardial cell metabolism with membrane dysfunction as indicators of necrosis/viability, 43 patients with evolving myocardial infarction and coronary arteriography had positron emission tomography using fluorodeoxyglucose (FDG) and the potassium analog 82Rb. Percent of heart showing FDG defects and 82Rb washout on sequential images indicating failure to retain the potassium analogue were visually assessed and quantified by automated software. Infarct size based on rubidium kinetics correlated closely with size and location on FDG images (visual r = 0.93, automated r = 0.82), suggesting that loss of cell membrane integrity for trapping the potassium analog 82Rb parallels loss of intracellular glucose metabolism, both comparable quantitative markers of myocardial necrosis/viability.

Experimental studies in animals have suggested that coronary flow reserve may be limited in patients with left ventricular hypertrophy (LVH). Accordingly, to noninvasively determine the effect of LVH on myocardial perfusion reserve, 25 patients, 9 with LVH and 16 controls, underwent positron imaging with rubidium-82 (82Rb) (30-55 mCi) or nitrogen-13 (13N) ammonia (12-19 mCi) at rest and following intravenous dipyridamole and handgrip stress. LVH was documented by echocardiographic and/or electrocardiographic measurements. LVH patients had either no chest pain (n = 8) and/or a normal coronary angiogram (n = 6). Nine simultaneous transaxial images were acquired, and the mean ratio of stress to rest activity (S:R), based on all regions for each heart, was calculated as an estimate of myocardial perfusion reserve. There were no regional differences in activity (i.e., perfusion defects) in any of the studies. S:R averaged 1.41 +/- 0.10 (s.d.) for controls and 1.06 +/- 0.09 for patients with LVH (p less than 0.0001). These data provide support for an abnormality in perfusion reserve in patients with LVH.