Comparison of cardiac magnetic resonance imaging and fluorodeoxyglucose positron emission tomography in the assessment of myocardial viability: meta-analysis and systematic review.

AIM: Contrast-enhanced cardiac magnetic resonance (Ce-CMR) and Fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) are frequently utilized in clinical practice to assess myocardial viability. However, studies evaluating direct comparison between Ce-CMR and FDG-PET have a smaller sample size, and no clear distinction between the two imaging modalities has been defined. To address this gap, we conducted a meta-analysis of studies comparing Ce-CMR and FDG-PET for the assessment of myocardial viability. METHODS: We searched PubMed, EMBASE, Scopus, and Web of Science databases from their inception to 4/20/2022 with search terms "viability" AND "heart diseases" AND "cardiac magnetic resonance imaging" AND "positron-emission tomography." We extracted patient characteristics, segment level viability assessment according to Ce-CMR and FDG-PET, and change in regional wall motion abnormalities (RWMA) at follow-up. RESULTS: We included four studies in the meta-analysis which provided viability assessment with Ce-CMR and FDG-PET in all patients and change in RWMA at follow-up. There were 82 patients among the four included studies, and 585 segments were compared for viability assessment. There were 59 (72%) males, and mean age was 65 years. The sensitivity (95% confidence interval-CI) and specificity (CI) of Ce-CMR for predicting myocardial recovery were 0.88 (0.66-0.96) and 0.64 (0.49-0.77), respectively. The sensitivity (CI) and specificity (CI) of FDG-PET for predicting myocardial recovery were 0.91 (0.63-0.99) and 0.67 (0.49-0.81), respectively. CONCLUSION: FDG-PET and Ce-CMR have comparable diagnostic parameters in myocardial viability assessment and are consistent with prior research.

Does reduced lung diffusing capacity for carbon monoxide predict the presence of pulmonary hypertension?

OBJECTIVE: The objective of this study was to determine whether reduced lung diffusing capacity for carbon monoxide (DLCO) predicts the presence of pulmonary hypertension (PH) in heterogeneous group of patients. METHODS: Consecutive patients who underwent pulmonary function and transthoracic echocardiographic testing within a 6-month period were retrospectively identified by chart review. Right ventricular systolic pressure (RVSP) was measured using Doppler echocardiography. PH was defined as a RVSP >30 mm Hg. Patients were divided into 2 major groups: those whose RVSP was < or =30 mm Hg and those whose RVSP was >30 mm Hg. PH was classified as mild (RVSP = 31-40 mm Hg), moderate (RSVP = 41-60 mm Hg) and severe (RVSP >60 mm Hg). RESULTS: A total of 398 patients were entered into the study: 264 (66.3%) with PH and 134 (33.7%) without PH. Patients with PH were older, had a lower mean percentage of predicted values for forced vital capacity (%FVC), for DLCO (%DLCO) and for DLCO corrected for alveolar volume (%DLCO/VA) than those without PH. Multivariate analysis identified age and %FVC as independent predictors of PH [odds ratios and 95% confidence intervals of 1.038 (1.020-1.056) and 0.972 (0.955-0.988), respectively]. There was a weak, but significant negative correlation between RVSP and %DLCO (r = -0.205, P = 0.001), but there was no correlation between RVSP and %DLCO/VA. Neither %DLCO nor %DLCO/VA was found to be independent predictors of PH. CONCLUSION: In a heterogeneous group of patients, %DLCO and %DLCO/VA do not independently predict the presence of PH.

Therapeutic challenges in combined apical ballooning syndrome and acute pulmonary decompensation.

Apical ballooning syndrome (ABS) is increasingly diagnosed in critical care settings. Widespread application of echocardiography and cardiac enzyme testing has increased its recognition. Our experience of 4 subjects illustrates the association of ABS with a wide spectrum of acute pulmonary disorders seen in critical care settings. All had ABS proven by normal coronary angiogram and subsequent normalization of left ventricular dysfunction. Bronchospasm due to chronic obstructive pulmonary disease exacerbation or cardiac failure warrants the use of beta agonists. ABS, on the other hand, being caused by excess sympathetic activity could potentially improve with beta blockade. Coexistence of ABS and pulmonary disease in critical-care settings presents unique therapeutic challenges and outcomes can be optimized by judicious use of available medical options.

Outcomes in patients with abnormal myocardial perfusion imaging and normal coronary angiogram.

A subset of subjects undergoing myocardial perfusion imaging has perfusion abnormalities that are subsequently labeled false positive based on coronary angiography. We evaluated the long-term prevalence of cardiovascular events in these patients. We retrospectively identified 48 patients who had reversible perfusion abnormalities with myocardial perfusion imaging and normal coronary angiography. Patients with known coronary artery disease, left ventricular dysfunction, valvular disease, and cardiomyopathy were excluded. Patient follow-up, conducted for at least 3 (mean interval, 7.4) years from the index myocardial perfusion imaging, was accomplished by a review of medical records and telephone interviews. Study endpoints were cardiovascular events defined as sudden cardiac death, myocardial infarction, percutaneous coronary revascularization, coronary artery bypass grafting, and cerebrovascular or peripheral revascularization. Thirty-one percent (15 of 48) of the patients had cardiovascular events. Six of the 48 patients had coronary events. These patients had abnormal myocardial perfusion imaging and normal coronary angiogram. The time between myocardial perfusion imaging and coronary event was 0.5 to 8.67 years. There was a strong correlation between the regions of original perfusion abnormality and the ultimate coronary ischemia or revascularization. Abnormal findings on myocardial perfusion imaging may predict a higher prevalence of coronary and peripheral vascular events than suggested by a normal coronary angiogram.

Oxidative stress contributes to pulmonary hypertension in the transgenic (mRen2)27 rat.

The transgenic (mRen2)27 (Ren2) rat overexpresses mouse renin in extrarenal tissues, causing increased local synthesis of ANG II, oxidative stress, and hypertension. However, little is known about the role of oxidative stress induced by the tissue renin-angiotensin system (RAS) as a contributing factor in pulmonary hypertension (PH). Using male Ren2 rats, we test the hypothesis that lung tissue RAS overexpression and resultant oxidative stress contribute to PH and pulmonary vascular remodeling. Mean arterial pressure (MAP), right ventricular systolic pressure (RVSP), and wall thickness of small pulmonary arteries (PA), as well as intrapulmonary NADPH oxidase activity and subunit protein expression and reactive oxygen species (ROS), were compared in age-matched Ren2 and Sprague-Dawley (SD) rats pretreated with the SOD/catalase mimetic tempol for 21 days. In placebo-treated Ren2 rats, MAP and RVSP, as well as intrapulmonary NADPH oxidase activity and subunits (Nox2, p22phox, and Rac-1) and ROS, were elevated compared with placebo-treated SD rats (P < 0.05). Tempol decreased RVSP (P < 0.05), but not MAP, in Ren2 rats. Tempol also reduced intrapulmonary NADPH oxidase activity, Nox2, p22phox, and Rac-1 protein expression, and ROS in Ren2 rats (P < 0.05). Compared with SD rats, the cross-sectional surface area of small PA was 38% greater (P < 0.001) and luminal surface area was 54% less (P < 0.001) in Ren2 rats. Wall surface area was reduced and luminal area was increased in tempol-treated SD and Ren2 rats compared with untreated controls (P < 0.05). Collectively, the results of this investigation support a seminal role for enhanced tissue RAS/oxidative stress as factors in development of PH and pulmonary vascular remodeling.