Identifying the Infarct-Related Artery in Patients With Non-ST-Segment-Elevation Myocardial Infarction.

BACKGROUND: Determining the infarct-related artery (IRA) in non-ST-segment-elevation myocardial infarction (MI) can be challenging. Delayed-enhancement cardiac magnetic resonance (DE-CMR) can accurately identify small MIs. The purpose of this study was to determine whether DE-CMR improves the ability to identify the IRA in patients with non-ST-segment-elevation MI. METHODS AND RESULTS: In this 3-center, prospective study, we enrolled 114 patients presenting with their first MI. Patients underwent DE-CMR followed by coronary angiography. The interventional cardiologist was blinded to the DE-CMR results. Later, coronary angiography and DE-CMR images were reviewed independently and blindly for identification of the IRA. The pattern of DE-CMR hyperenhancement was also used to determine whether there was a nonischemic pathogenesis for myocardial necrosis. The IRA was not identifiable by coronary angiography in 37% of patients (n=42). In these, the IRA or a new noncoronary artery disease diagnosis was identified by DE-CMR in 60% and 19% of patients, respectively. Even in patients with an IRA determined by coronary angiography, a different IRA or a noncoronary artery disease diagnosis was identified by DE-CMR in 14% and 13%, respectively. Overall, DE-CMR led to a new IRA diagnosis in 31%, a diagnosis of nonischemic pathogenesis in 15%, or either in 46% (95% CI, 37%-55%) of patients. Of 55 patients undergoing revascularization, 27% had revascularization solely to nonculprit coronary artery territories as determined by DE-CMR. CONCLUSIONS: Identification of the IRA by coronary angiography can be challenging in patients with non-ST-segment-elevation MI. In nearly half, DE-CMR may lead to a new IRA diagnosis or elucidate a nonischemic pathogenesis. Revascularization solely of coronary arteries that are believed to be nonculprit arteries by DE-CMR is not uncommon.

Biochar from green waste for phosphate removal with subsequent disposal.

Biochar prepared from cotton stalk solid waste provides a new material for contaminant removal. In the present study, experiments were conducted to investigate the removal of phosphate from aqueous solution by cotton stalk biochar (CSB). The characterization of CSB & phosphate adsorbed biochar (PCSB) were done to substantiate the adsorption of phosphate on CSB surface. FT-IR studies disclosed the functional groups present in CSB and supported adsorption phenomena. Scanning electron microscope showed the porous nature of CSB and EDS measurements justified the phosphate adsorption process. XRD analysis revealed that the calcium and magnesium ions of CSB were also responsible for adsorption process. Experimental results fitted nicely with the heterogeneous isotherm models viz Freundlich and Temkin isotherm. The calculated Freundlich constant (n) suggested the cooperative adsorption. The heat of adsorption calculated from Temkin isotherm indicated the process to be exothermic in nature. The free energy of adsorption calculated from equilibrium studies justified physical as well as chemical means of adsorption. Hence CSB serves as a good adsorptive material and can provide viable solution for environmental protection. However, discharging active site depleted CSB to environment may pose subsequent problems. To combat the same, the PCSB was tested as nutrient enhancer for plant growth in soil and population multipliers of microbes in microbial fuel cells-a device for power generation. The disposal study concluded the feasibility of safe PCSB removal.

Lateral MI Explains the Presence of Prominent R Wave (R ≥ S) in V1.

AIMS: It is necessary to clarify if the presence of a prominent R wave in V1, in post-myocardial infarction (MI) patients, is due to the involvement of the posterior wall (currently inferobasal segment) or the lateral wall (as has been demonstrated recently by electrocardiographic contrast-enhanced cardiac magnetic resonance [ECG-CE-CMR] correlations studies). METHODS: In 155 patients with inferolateral zone MI, as detected by CE-CMR, the following ECG parameters were evaluated and correlated with MI location according to CE-CMR: R/S ratio in V1 ≥ 1 (classic criteria for posterior MI), R/S ratio in V1 ≥ 0.5, and R in V1 ≥ 3 mm. RESULTS: R/S ≥ 1 criterion: Present in 20 cases: 3 of lateral MI, 17 of inferolateral MI, 0 of inferior MI. Absent in 135 cases, 81 of lateral/inferolateral MI (28/53), 54 of inferior MI (SE 19.8%, SP 100%). R/S ≥ 0.5 criterion: Present in 47 cases: 6 of lateral MI, 39 of inferolateral MI, 2 of inferior MI. Absent in 108 cases, 56 of lateral/inferolateral MI (25/31), 52 of inferior MI (SE 44.6%, SP 96.4%). R ≥ 3 mm criterion: Present in 30 cases: 5 of IM lateral, 23 of inferolateral MI, 2 of inferior MI. Absent in 125 cases, 73 lateral/inferolateral MI (26/47), 52 inferior MI (SE 27.7%, SP 96.4%). CONCLUSIONS: The presence of prominent the R wave in V1 is due to the lateral MI and not to the involvement of inferobasal segment of inferior wall (old posterior wall).

Prognostic variables for clinical outcomes in valvular heart disease patients with moderate to severe secondary tricuspid regurgitation.

BACKGROUND AND AIM OF THE STUDY: Secondary tricuspid regurgitation (STR) is frequently seen in cardiology practice. Currently, few data are available on the prognostic variables associated with moderate or severe STR on death and progression to valve surgery. Hence, the study aim was to identify these prognostic variables. METHODS: In this retrospective study, patients with at least moderate STR were identified from an ongoing database and followed until death, any valvular heart surgery, or the end of the study. Clinical and echocardiographic variables including age, gender, coronary artery disease, device implantation (defibrillator or pacemaker), pulmonary disease, left ventricular ejection fraction, right ventricular size, right ventricular systolic pressure (RVSP), STR severity and concomitant valve disease were recorded. End-points were death and valve surgery. RESULTS: The average age of the 92 study participants was 68 +/- 16 years. During a mean follow up of 43 +/- 24 months, there were 13 deaths (14%) and 12 surgeries (13%). In multivariate analysis, both an elevated RVSP and device implantation were significant predictors of death (p = 0.0038 and 0.0487, respectively). Only an elevated RVSP was predictive of surgery (p = 0.05) and surgery-free survival (p = 0.0005). A RVSP > 48 mmHg had a hazard ratio of 3.93 (p = 0.0012) and a high diagnostic accuracy for predicting death, with an area under the receiver operating characteristic curve of 0.73. CONCLUSION: In patients with valvular heart disease and at least moderate STR, an elevated RVSP of at least 48 mmHg was associated with significantly increased mortality and decreased surgery-free survival.

Heart failure with a normal left ventricular ejection fraction: epidemiology, pathophysiology, diagnosis and management.

Heart failure (HF) with a normal left ventricular (LV) ejection fraction (HFNEF) occurs in 40-71% of patients with HF and carries a prognosis similar to that of HF with a reduced LV ejection fraction (LVEF). The pathophysiology of HFNEF is distinct from that of HF with a reduced LVEF and is characterized by impaired relaxation of myocardium, LV stiffness and, in many cases, increased arterial stiffness. Systemic hypertension accounts for most cases of HFNEF in the United States. Those with HFNEF tend to be older and obese. Diabetes mellitus and atrial fibrillation occur with disproportionately high frequency in HFNEF. The diagnosis of HFNEF requires the presence of symptoms or signs of HF, a normal or near-normal LVEF and evidence of LV diastolic dysfunction based on cardiac catheterization or Doppler echocardiographic techniques and/or elevation of plasma natriuretic peptide levels. Current guidelines for management of HFNEF include control of systolic and diastolic hypertension, control of the ventricular rate in patients with atrial fibrillation and judicious use of diuretics. In selected cases, coronary revascularization or restoration of sinus rhythm in those with atrial fibrillation may be indicated. To date, no drug or drug group has consistently improved survival in HFNEF. For this reason and because of the poor long-term prognosis, preventative measures and effective treatment of underlying causes and precipitating factors are particularly important in avoiding HF exacerbations in patients with HFNEF.

Tachycardia-induced cardiomyopathy: evaluation and therapeutic options.

Tachycardia-induced cardiomyopathy is caused by sustained rapid ventricular rates and is one of the well-known forms of reversible myocardial dysfunction. The diagnosis is usually made retrospectively after marked improvement in systolic function is noted following control of the heart rate. Physicians should be aware that patients with seemingly idiopathic systolic dysfunction may have tachycardia-induced cardiomyopathy and that controlling the heart rate may result in improvement or even complete restoration of systolic function.

Identifying the etiology: a systematic approach using delayed-enhancement cardiovascular magnetic resonance.

In patients who have heart failure, treatment and survival are directly related to the cause. Clinically, as a practical first step, patients are classified as having either ischemic or non-ischemic cardiomyopathy, a delineation usually based on the presence or absence of epicardial coronary artery disease. However, this approach does not account for patients with non-ischemic cardiomyopathy who also have coronary artery disease, which may be either incidental or partly contributing to myocardial dysfunction (mixed cardiomyopathy). By allowing direct assessment of the myocardium, delayed-enhancement cardiovascular magnetic resonance (DE-CMR) may aid in addressing these conundrums. This article explores the use of DE-CMR in identifying ischemic and non-ischemic myopathic processes and details a systematic approach to determine the cause of cardiomyopathy.

Sildenafil promotes ischemia-induced angiogenesis through a PKG-dependent pathway.

BACKGROUND: Peripheral artery disease (PAD) is a prevalent cardiovascular disorder that results in tissue ischemia which can progress to critical limb ischemia. Restoration of tissue perfusion in the setting of chronic ischemia through stimulation of arteriogenesis and angiogenesis remains a key therapeutic target for PAD. However, experimental therapeutics, including growth factor and gene therapy, have had little clinical success indicating the need for a better understanding of molecular pathways required for therapeutic angiogenesis. METHODS AND RESULTS: Here we report that phosphodiesterase-5 inhibition by sildenafil significantly increases vascular perfusion, tissue blood flow, and vascular density during chronic ischemia of the mouse hind limb. Importantly, sildenafil therapy did not alter any of these parameters in nonischemic limbs. Sildenafil increased tissue cGMP levels independently of increases in nitric oxide production, and sildenafil therapy stimulated angiogenesis in ischemic limbs of eNOS-/- and iNOS-/- mice. Lastly, sildenafil-mediated angiogenic activity was blocked by inhibition of protein kinase G using the PKG antagonist DT-3. CONCLUSIONS: These data demonstrate that sildenafil therapy results in increased angiogenic activity through a PKG-dependent pathway that is independent of nitric oxide production or NOS activity and identify the angiogenic therapeutic potential of sildenafil for critical limb ischemia.

Differential angiogenic regulation of experimental colitis.

Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders of the intestinal tract with unknown multifactorial etiology that, among other things, result in alteration and dysfunction of the intestinal microvasculature. Clinical observations of increased colon microvascular density during IBD have been made. However, there have been no reports investigating the physiological or pathological importance of angiogenic stimulation during the development of intestinal inflammation. Here we report that the dextran sodium sulfate and CD4+CD45RBhigh T-cell transfer models of colitis stimulate angiogenesis that results in increased blood vessel density concomitant with increased histopathology, suggesting that the neovasculature contributes to tissue damage during colitis. We also show that leukocyte infiltration is an obligatory requirement for the stimulation of angiogenesis. The angiogenic response during experimental colitis was differentially regulated in that the production of various angiogenic mediators was diverse between the two models with only a small group of molecules being similarly controlled. Importantly, treatment with the anti-angiogenic agent thalidomide or ATN-161 significantly reduced angiogenic activity and associated tissue histopathology during experimental colitis. Our findings identify a direct pathological link between angiogenesis and the development of experimental colitis, representing a novel therapeutic target for IBD.