Prophylactic use of carvedilol to prevent ventricular dysfunction in patients with cancer treated with doxorubicin

Objective: Deterioration in ventricular function is often observed in patients treated with anthracyclines for cancer. There is a paucity of evidence on interventions that might provide cardio-protection. We investigated whether prophylactic use of carvedilol can prevent doxorubicin-induced cardiotoxicity and whether any observed effect is dose related. Methods: A prospective, randomized, double-blind study in patients treated with doxorubicin, comparing placebo (n = 38) with different doses of carvedilol [6.25 mg/day (n = 41), 12.5 mg/day (n = 38) or 25 mg/day (n = 37)]. The primary endpoint was the measured change in left ventricular ejection fraction (LVEF) from baseline to 6 months. Results: LVEF decreased from 62 ± 5% at baseline to 58 ± 7% at 6-months (p = 0.002) in patients assigned to placebo but no statistically significant changes were observed in any of the 3 carvedilol groups. At 6 months, only one of 116 patients (1%) assigned to carvedilol had an LVEF < 50% compared to four of the 38 assigned to placebo (11%), (p = 0.013). No significant differences were noted between carvedilol and placebo in terms of the development of diastolic dysfunction, clinically overt heart failure or death. Conclusions: Carvedilol might prevent deterioration in LVEF in cancer patients treated with doxorubicin. This effect may not be dose related within the studied range

Uncommon cause of complicated myocardial infarction with normal coronary arteries in a Saudi patient

A case of a young Saudi patient with a previous diagnosis of bronchial asthma, nasal polyps, and chronic smoker, presented with atypical chest pain, elevated serum troponin and borderline ischemic electrocardiogram (ECG) changes, with no significant regional wall motion abnormalities at bedside echocardiography is reported. The patient was admitted to the coronary care unit for continuous monitoring as possible acute coronary syndrome, non-ST elevation myocardial infarction (STEMI). One hour after admission, the patient had ventricular fibrillation (VF) cardiac arrest that required three DC shocks and amiodarone bolus before returning of spontaneous circulation, which followed the fourth shock. The resuscitation took 15 minutes of cardiopulmonary resuscitation (CPR). An immediate 12-leads ECG showed significant ST elevation in precordial leads that mandate an urgent coronary angiogram that revealed patent coronary arteries, therefore spasm of normal coronary arteries was postulated as the operative factor. The cardiac magnetic resonance image (MRI) showed a picture of transmural anterior myocardial infarction, which correlates with the follow up echocardiogram reporting hypokinetic anterior wall. A complete history was taken and no use of illicit drugs or alcohol was found. The unusual presentation in such a patient with evidence of extensive anterior STEMI and normal coronary arteries raise the thought of considering uncommon causes. In view of previous medical history and laboratory evidence of eosinophilia, Kounis syndrome was considered dominant in the differential diagnosis. Keywords: Coronary, Myocardial, infarction, Kouni

Serum insulin-like growth factor binding protein-1 (IGFBP-1) phosphorylation status in subjects with and without ischaemic heart disease.

Insulin-like growth factor binding protein-1 (IGFBP-1) modulates the activity of IGF-I. It exists in serum as phosphorylated and less phosphorylated forms. We wished to measure serum levels of both these forms of IGFBP-1, using a novel assay, in subjects with, or without ischaemic heart disease (IHD)

Serum insulin-like growth factor binding protein-1 (IGFBP-1) phosphorylation status in subjects with and without ischaemic heart disease

Background: Insulin-like growth factor binding protein-1 (IGFBP-1) modulates the activity of IGF-I. It exists in serum as phosphorylated and less phosphorylated forms. We wished to measure serum levels of both these forms of IGFBP-1, using a novel assay, in subjects with, or without ischaemic heart disease (IHD). Methods: We measured serum concentrations of the phosphorylated and less phosphorylated forms of IGFBP-1 in 75 subjects (36 with and 39 without IHD). Two immunoassays were used, one which detects non-, and less-phosphorylated forms (LpIGFBP-1), and another which specifically detects the serine phosphorylated form of IGFBP-1 (pIGFBP-1). Results: LpIGFBP-1 concentrations were significantly higher in subjects without IHD than in those with IHD (5.3 +/- 0.5 mu g/L vs. 2.7 +/- 0.4 mu g/L, p < 0.001). pIGFBP-1 levels were also significantly higher in subjects without IHD compared to those with IHD (33.3 +/- 2.0 mu g/L vs. 25.3 +/- 2.2 mu g/L, p < 0.01). The correlation between LpIGFBP-1 and pIGFBP-1 for all subjects was (r = 0.71, p < 0.001). This association was stronger in subjects without IHD (r = 0.76, p < 0.001) than for those with IHD (r = 0.60, p < 0.001). A significant negative association was observed between IGF-I and the ratio between the two forms (r = -0.45, p < 0.0001). Receiver-Operating Characteristic (ROC) curve showed the highest area under the curve for LpIGFBP-1 (0.75) [95% CI: 0.63-0.86] and optimum cut-off value of 2.83 mu g/L with 75% sensitivity and 74% specificity. Conclusions: We propose that low serum concentrations of IGFBP-1 forms could be a marker of coronary risk, and the LpIGFBP-1: pIGFBP-1 ratio may be an index of biologically active IGF-

The prognostic impact of hyperglycemia on clinical outcomes of acute heart failure: Insights from the heart function assessment registry trial in Saudi Arabia

Background: The prognostic impact of hyperglycemia (HG) in acute heart failure (AHF) is controversial. Our aim is to examine the impact of HG on short- and long-term survival in AHF patients. Methods: Data from the Heart Function Assessment Registry Trial in Saudi Arabia (HEARTS) for patients who had available random blood sugar (RBS) were analyzed. The enrollment period was from October 2009 to December 2010. Comparisons were performed according to the RBS levels on admission as either <11.1 mmol/L or ≥11.1 mmol/L. Primary outcomes were hospital adverse events and short- and long-term mortality rates. Results: A total of 2511 patients were analyzed. Of those, 728 (29%) had HG. Compared to non-HG patients, hyperglycemics had higher rates of hospital, 30-day, and 1-year mortality rates (8.8% vs. 5.6%; p = 0.003, 10.4% vs. 7.2%; p = 0.007, and 21.8% vs. 18.4%; p = 0.04, respectively). There were no differences between the two groups in 2- or 3-year mortality rates. After adjustment for relevant confounders, HG remained an independent predictor for hospital and 30-day mortality [odds ratio (OR) = 1.6; 95% confidence interval (CI) 1.07–2.42; p = 0.021, and OR = 1.55; 95% CI 1.07–2.25; p = 0.02, respectively]. Conclusion: HG on admission is independently associated with hospital and short-term mortality in AHF patients. Future research should focus on examining the impact of tight glycemic control on outcomes of AHF patients. Keywords: Acute heart failure, HEARTS, Hyperglycemia, Mortality, Random blood glucos

Disparities in Health Care Delivery and Hospital Outcomes between Non-Saudis and Saudi Nationals Presenting with Acute Coronary Syndromes in Saudi Arabia

<div><p>Background</p><p>Saudi Arabia has a non-Saudi workers population. We investigated the differences and similarities of expatriate non-Saudi patients (NS) and Saudi nationals (SN) presenting with acute coronary syndromes (ACS) with respect to therapies and clinical outcomes.</p><p>Methods</p><p>The study evaluated 2031 of the 5055 ACS patients enrolled in the Saudi Project for Assessment of Acute Coronary Syndrome (SPACE) from 2005 to 2007. Propensity score matching and logistic regression analysis were performed to account for major imbalances in age and sex in the two groups.</p><p>Results</p><p>The mean patient age was 56.2±9.8, and 83.5% of the study cohort were male. SN were more likely to have risk factors of atherosclerosis. ST-elevation MI (STEMI) was the most common ACS presentation in NS, while non-ST ACS was more common in SN. The median symptom-to-door time was significantly greater in NS patients (Median 175 min (197) vs. 130 min (167), p=0.027). The only difference in pharmacological therapies between the two groups was that NS were more likely to receive fibrinolytic therapy. NS were less likely than SN to undergo percutaneous coronary interventions (PCI; 32.6% vs. 42.8%, p=0.0001) or primary PCI (7.8% vs. 22.8%, p<0.001). Hospital mortality, cardiogenic shock, and heart failure were significantly higher in NS compared to SN. After adjusting for baseline variables and therapies, the odds ratios for hospital mortality and cardiogenic shock in NS were 2.9 (95% CI 1.5–6.2, p=0.004) and 2.8 (95% CI 1.5–4.9, p<0.001), respectively.</p><p>Conclusion</p><p>Our findings indicate disparities in hospital care between NS and SN ACS patients. NS patients had worse hospital outcomes, which may reflect unequal health coverage and access-to-care issues.</p></div