Primary Open Versus Closed Implantation Strategy for Totally Implantable Venous Access Ports: The Multicentre Randomized Controlled PORTAS-3 Trial (DRKS 00004900).

OBJECTIVES: PORTAS-3 was designed to compare the frequency of pneumothorax or haemothorax in a primary open versus closed strategy for port implantation. BACKGROUND DATA: The implantation strategy for totally implantable venous access ports with the optimal benefit/risk ratio remains unclear. METHODS: PORTAS-3 was a multicentre, randomized, controlled, parallel-group superiority trial. Adult patients with oncological disease scheduled for elective port implantation were randomized to a primary open or closed strategy. Primary endpoint was the rate of pneumothorax or haemothorax. Assuming a difference of 2.5% between the 2 groups, a sample size of 1154 patients was needed to prove superiority of the open group. A logistic regression model after the intention-to-treat principle was applied for analysis of the primary endpoint. RESULTS: Between November 9, 2014 and September 5, 2016, 1205 patients were randomized. Of these, 1159 (open n = 583; closed n = 576) were finally analyzed. The rate of pneumothorax or haemothorax was significantly reduced with the open strategy [odds ratio 0.27, 95% confidence interval (CI) 0.09-0.88; P = 0.029]. Operation time was shorter for the closed strategy. Primary success rates, tolerability, morbidity, dose rate of radiation, and 30-day mortality did not differ significantly between the groups. CONCLUSION: A primary open strategy by cut-down of the cephalic vein, if necessary enhanced by a modified Seldinger technique, reduces the frequency of pneumothorax or haemothorax after central venous port implantation significantly compared with a closed strategy by primary puncture of the subclavian vein without routine sonographic guidance. Therefore, open surgical cut-down should be the reference standard for port implantation in comparable cohorts. TRIAL REGISTRATION: German Clinical Trials Register DRKS 00004900.

Cholesterol crystal embolization following plaque rupture: a systemic disease with unusual features.

Cholesterol crystal embolic (CCE) syndrome is often a clinically challenging condition that has a poor prognostic implication. It is a result of plaque rupture with release of cholesterol crystals into the circulation that embolize into various tissue organs. Plaque rupture seems to be triggered by an expanding necrotic core during cholesterol crystallization forming sharp tipped crystals that perforate and tear the fibrous cap. Embolizing cholesterol crystals then initiate both local and systemic inflammation that eventually lead to vascular fibrosis and obstruction causing symptoms that can mimic other vasculitic conditions. In fact, animal studies have demonstrated that cholesterol crystals can trigger an inflammatory response via NLRP3 inflammasome similar to that seen with gout. The diagnosis of CCE syndrome often requires a high suspicion of the condition. Serum inflammation biomarkers including elevated sedimentation rate, abnormal renal function tests and eosinophilia are useful but non-specific. Common target organ involvement includes the skin, kidney, and brain. Various testing including fundoscopic eye examination and other non-invasive procedures such as trans-esophageal echocardiography and magnetic resonance imaging may be helpful in identifying the embolic source. Treatment includes aspirin and clopidogrel, high dose statin and possibly steroids. In rare cases, mechanical intervention using covered stents may help isolate the ruptured plaque. Anticoagulation with warfarin is not recommended and might even be harmful. Overall, CCE syndrome is usually a harbinger of extensive and unstable atherosclerotic disease that is often associated with acute cardiovascular events.

Acute changes in left ventricular diastolic function: cigarette smoking versus nicotine gum.

BACKGROUND: Echocardiographic evidence of diastolic dysfunction has been demonstrated during acute cigarette smoking in patients with coronary artery disease. Similar studies in healthy patients have shown conflicting results. Furthermore, it is unclear whether nicotine or some other cigarette-related substance is responsible for these observations. HYPOTHESIS: The purpose of the study was to confirm or refute acute effects of cigarette smoking on diastolic function in healthy patients and to compare diastolic effects of a cigarette to smokeless nicotine delivery (nicotine gum). METHODS: In all, 27 healthy volunteers were self-assigned into one of two cohorts. A baseline echocardiogram was performed in all patients. The first cohort proceeded to smoke a cigarette and the second to chew a piece of nicotine gum. Within minutes after exposure, another echocardiogram was performed. Traditional measures of diastolic function were compared before and after substance exposure by paired t-tests. RESULTS: The cigarette cohort showed echocardiographic evidence of diastolic dysfunction after smoking. The E:A ratio (time integral) decreased from 2.95 to 2.22 (p < 0.002). Atrial reversal pulmonary velocity, atrial reversal duration, and color flow propagation all showed statistically significant alterations (p < 0.05). The nicotine gum cohort showed no change in traditional diastolic parameters. CONCLUSIONS: Diastolic function is impaired during acute exposure to cigarette smoke but unchanged after exposure to nicotine gum. It is therefore unlikely that nicotine alone is responsible for cigarette-induced acute diastolic dysfunction.

Should angiotensin receptor blockers be added to angiotensin-converting enzyme inhibitors in the treatment of heart failure?

Angiotensin-converting enzyme (ACE) inhibitors have been the cornerstone of treatment of heart failure. Angiotensin receptor blockers (ARBs) remain an attractive alternative in heart failure patients intolerant of ACE inhibitors. The addition of ARBs to ACE inhibitors in the context of stable heart failure may lead to additional clinical benefits. This is in contrast to heart failure complicating acute myocardial infarction, in which it does not offer any therapeutic advantage.

Primary cardiac pleomorphic sarcoma presenting as back pain in an 18-year-old man.

Soft-tissue sarcoma is the most prevalent primary malignant cardiac tumor. This sarcoma usually presents with cardiac manifestations secondary to local obstruction or arrhythmias; very rarely does it present with initial symptoms of distant metastasis. We discuss the unusual case of an 18-year-old man who emergently presented with acute-on-chronic back pain. Imaging revealed a lesion on the 12th thoracic vertebra and a large mass arising from the left atrium. The cardiac mass was resected, and immunohistochemical analysis revealed it to be a pleomorphic sarcoma that had metastasized to the spine. The patient died 2 years later of diffuse metastases. In addition to the patient's case, we discuss the nature and treatment of cardiac sarcoma.

Use of antihypertensive drugs during pregnancy and lactation.

The decision to treat elevated arterial pressure in pregnancy depends on the risk and benefits imposed on the mother and the fetus. Treatment for mild-to-moderate hypertension during pregnancy may not reduce maternal or fetal risk. Severe hypertension, on the other hand, should be treated to decrease maternal risk. Methyldopa and beta-adrenoceptor antagonists have been used most extensively. In acute severe hypertension, intravenous labetalol or oral nifedipine are reasonable choices.

Inflammation in high blood pressure: a clinician perspective.

Hypertension is one of the most important contributors to atherosclerosis. A possible link between inflammation and elevated blood pressure has been suggested by several cross-sectional and longitudinal studies. Possible mechanisms include an imbalance between vasoconstrictors and vasodilators, amplified thrombogenesis and platelet activation, and perhaps a direct effect of inflammatory mediators. C-reactive protein (CRP), an inflammatory cytokine, may play an essential role in vascular inflammation and can directly decrease the production of nitric oxide, a vasocodilator. Angiotensin II (Ang II) up-regulates several inflammatory cytokines, leukocyte adhesion molecules, and chemokines through the activation of the nuclear factor-kappa B leading to a decrease in the bioavailability of vasodilators. The increase in oxidative stress and endothelin-1 production through Ang II may further contribute to vasoconstriction. Adipose tissue can add to the production of CRP and creates a prothrombotic state. The presence of low-grade inflammation, especially elevations of CRP, can help predict the risk of future cardiovascular events and is associated with target organ damage in hypertensive individuals. Angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-adrenoreceptor antagonists, and, to a lesser degree calcium channel antagonists, have shown efficacy in reducing CRP. Lifestyle changes such as exercise, weight loss, and tobacco cessation have also shown a similar efficacy. Whether targeting inflammation in the treatment of uncomplicated hypertension can alter the natural history of the disease or lead to improved outcome has yet to be determined.