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Modification of Irene Vinagre's affiliation (Irene Vinagre, 19 March 2014)

The correct affiliation of Irene Vinagre is: 2 Endocrinology and Nutrition Department, Hospital de la Santa Creu i Sant Pau, C/ Mas Casanovas 90, Barcelona 08025, Spain 6 Universitat Autònoma de Barcelona, Barcelona, Spain read full comment

Comment on: Sánchez-Quesada et al. Cardiovascular Diabetology, 12:112

We need new terms to better explore emergent clinical settings (Carlos Musso, 24 February 2014)

The names we use to designate diseases in fact reduce them to just a handful of links (segment) belonging to what actually is a huge chain of patho-physiological processes (continuum), but this interpretative approach makes possible to analyze this segments and later develop strategies (treatments) which tend to solve or slow down them. Nevertheless, the extension of life expectancy, together with the development of various kinds of therapeutic treatments (antibiotics, dialysis, transplants, etc.) has given way to a singular phenomenon: the appearance of new clinical scenarios whose evolutionary course and response to conventional therapeutics are different from the previous ones, so the classical labels turn out to be insufficient for them (1-4).            ... read full comment

Comment on: Schnell et al. Cardiovascular Diabetology, 12:156

Appropriate survey design analysis and exclusion criteria are required to confirm the association between blood lead concentration and metabolic syndrome in Korean adults (Yangho Kim, 27 June 2013)

Authors:... read full comment

Comment on: Rhee et al. Cardiovascular Diabetology, 12:9

Addressing predisease conditions (clinical triggers for chronic disease): A pathway for primary prevention of disease. (Alok Gupta, 09 March 2013)

Birth is usually followed by natural death. A disease can often hasten death. Predisease conditions, covertly present decades earlier [1], have been thought to promote early death, by insidiously converting into overt disease over time. It is, however, also being recognized that predisease conditions like prediabetes and prehypertension, do not only have a high prevalence among healthy adults in the United States [2,3], but also place these healthy individuals on an accelerated pathway for cardiovascular adverse events [4]. This risk appears to begin with an enlargement of the waist circumference, deposition adipose tissue in ectopic locations (visceral, liver and muscle), and adipose tissue dysfunction leading to worsening insulin resistance and/or systemic inflammation [5,6]. The early... read full comment

Comment on: Gupta et al. Cardiovascular Diabetology, 12:23

Corrigendum (Christa Buechler, 21 March 2012)

Fig. 1B on page 3:
We meanwhile recognized that an error had occurred during preparation part of figure 1 (i.e. figure 1B). This error, however, had no effect on scientific content and conclusions. In figure 1B the lower immunoblot is an erroneously duplication of the lower panel of figure 2B. The original adiponectin immunoblot looks quite similar and shows that LMW adiponectin is not altered 2 h after oral glucose uptake. Original blot can not be posted here and can be send upon request.
We deeply regret that these error occurred and are sorry for this inconvenience. read full comment

Comment on: Wurm et al. Cardiovascular Diabetology, 6:7

Correction (Rudolf de Boer, 21 March 2012)

The authors would like to correct that the drug substances used in this study was the vildagliptin analog PKF275-055. The authors apologize for the error. read full comment

Comment on: Yin et al. Cardiovascular Diabetology, 10:85

A mistake in the unit of fasting plasma glucose (Alexandra Kautzky-Willer, 05 July 2011)

Please note that the unit of Fasting plasma glucose in Table 2 and in Figure 2 is in (mg/dl) and not in (gm/dl). read full comment

Comment on: Rasul et al. Cardiovascular Diabetology, 10:55

Correction (Enrique Fisman, 13 June 2011)

Correction (posted on behalf of the... read full comment

Comment on: Dias et al. Cardiovascular Diabetology, 10:49

Mistake in Table 2 (Manuel A Gomez-Marcos, 13 June 2011)

In title "Bivariate correlations between IMT, risk factors and arterial stiffness measures (ambulatory arterial stiffness index, augmentation index and pulse wave velocity) in subjects with and without type 2 diabetes.

In second row, first column, delete "Univariate read full comment

Comment on: Gómez-Marcos et al. Cardiovascular Diabetology, 10:3

Correction (Kei Nakajima, 01 June 2011)

Figure 2
Q1 is highest quartile and Q4 is lowest quartile.

Figure 3 and Figure 4
Q1 is lowest quartile and Q4 is highest quartile. read full comment

Comment on: Nakajima et al. Cardiovascular Diabetology, 10:34

Carbohydrate-rich Diet Is The Likely Culprit For Insulin Resistance (Robert Su, 28 November 2010)

I thoroughly enjoyed reading this excellent article, “Hyperinsulinemia improves ischemic LV function in insulin resistant subjects” by Patrick M. Heck et al. Furthermore, the use of hyperinsulinemic euglycemic clamp (HEC) in this study prompts me to share my thought on the possible cause of insulin resistance.

Insulin resistance is a situation when the body, or more specifically, the cell, has built up resistance to the (endogenous) insulin produced by its pancreas, and cannot use the endogenous insulin for taking up and metabolizing the circulating glucose to produce energy, metabolites of glucose, glycogen, and fats. At the same time, the patient with insulin resistance continues to consume carbohydrates; his blood glucose level will rise accordingly. The more he... read full comment

Comment on: Heck et al. Cardiovascular Diabetology, 9:27

Erratum: (Alok Gupta, 06 October 2010)

Table 3 compares the seven obese participants with normal circadian BP variability with the eight obese participants who had abnormalities. The seven obese participants (BMI 32 kg/m2) who had normal circadian BP variability had normal glucose, hs-CRP, fibrinogen, triglycerides, HDL-C and cardiac risk ratios. In contrast the eight obese subjects with abnormal circadian BP variability exhibited (REPLACE majority WITH all) all of the CVD risk parameters outside of the desirable range.

The results from this study show that latent CVD risk in disease-free (healthy) obese adults assessed with no or low risk by conventional risk assessment methods, can be unmasked by simple non-invasive measures. The obese participants exhibiting normal circadian BP variability had... read full comment

Comment on: Gupta et al. Cardiovascular Diabetology, 9:58

It is the time to revisit dietary therapy for diabetes mellitus. (Robert Su, 17 September 2010)

Congratulations to Kurukulasuriya LR & Sowers JR of University of Missouri on their excellent analysis, “Therapies for type 2 diabetes: lowering HbA1c and associated cardiovascular risk factors”, to detail the desirable therapeutic and undesirable effects of each antidiabetes agent of each category, in terms of glycemic control, body weight, lipid level, and blood pressure parameters, all of which are significant cardiovascular risk factors. However, selecting a perfect antidibetes agent is hardly an easy decision, even equipped with such an excellent analysis. Both Kurukulasuriya & Sowers, as well as many physicians including the diabetes experts have continued to ignore an excellent therapeutic alternative to the pharmacotherapy.

Glycemic control is the key... read full comment

Comment on: Kurukulasuriya et al. Cardiovascular Diabetology, 9:45

Correction (yumi yumi, 22 February 2010)

I am Yumi Miyashita, the author of this article.

In the original report, the writing "A computer-assisted, least square method..." is wrong. The correct writing is "A computer-assisted,
read full comment

Comment on: Miyashita et al. Cardiovascular Diabetology, 7:16

Carbohydrate-restricted Diet for The Therapeutic Paradigm (Robert Su, 31 December 2009)

Robert Su, Pharm.B., M.D. Author, Carbohydrates Can Kill E-mail:

Congratulations to Doctors Node and Inoue on their excellent work to produce such an interesting and educational article.

In my literature review and personal experimentations, I have observed an axis of the excessive consumption of carbohydrates especially those high in glycemic indices and glycemic loads, the daily repeated postprandial hyperglycemia, the repeated postprandial inflammation with both acute and chronic pathological effects on cells, tissues, and organs. [1., 2, 3] The pathological role of hyperglycemia at least includes (1) inflammatory and pro-inflammatory, (2) vasoconstrictive (and hypertensive), (3) pro-... read full comment

Comment on: Node et al. Cardiovascular Diabetology, 8:23

Correction (Enrique Fisman, 17 December 2009)

After the publication of this manuscript, the authors discovered a mistake in the figure legends. In both legends the correct reference number should be 52 instead of 45. read full comment

Comment on: Fisman et al. Cardiovascular Diabetology, 8:38

Arterial Hypertension is under control if hepatic PPARs are well functioning. (Sergio Stagnaro, 09 December 2009)

from the clinical view-point, I agree with the data of this fascinating study. In fact, only when the lipid and glucose metabolism is under control, blood pressure can be in normal range. Now-a-days, the best method in assessing lipid and glucose metabolism is the bedside evaluation of liver PPARs (1-7). Accordingly, low caloric diet and regular physical exercise induced significant improvement in blood pressure, body mass index, waist-to-hip- circumference,without any change on drug prescription, but it brings about other paramount benifits (1). Let us consider, for instance, that one of the most active areas of metabolic research into potential treatments surrounds the role of nuclear receptors as a treatment target for both glucose and lipid metabolism. In addition, agonists... read full comment

Comment on: Zidek et al. Cardiovascular Diabetology, 8:51

Hypercoagulability, a physiological reaction to increased blood viscosity due to hypovolaemia (Simon Thornton, 14 May 2009)

Dear Sir,

I was very interested to read the recent article by Jax et al., (1) in the journal Cardiovascular Diabetology (2009; 8 (1): 24) entitled “Relevance of hemostatic risk factors on coronary morphology in patients with diabetes mellitus type 2” where the authors clearly show an increased thrombogenic state in diabetes associated with an increase in blood viscosity. Similar risk factors have been reported with hypertension and when this disease state is associated with diabetes the risk is even further increased (2). It is important to note that plasma viscosity correlates to the progression of coronary and peripheral artery diseases (3). Now the question could be asked whether the hypercoagulability is a symptom of the two disease states or a reaction to the... read full comment

Comment on: Jax et al. Cardiovascular Diabetology, 8:24

Biophysical-Semeiotic Bedside Evaluation of Leptin. (Sergio Stagnaro, 29 November 2007)

Sirs,Leptin receptors are highly expressed in areas of the hypothalamus known to be important in regulating body weight, as well as in T lymphocytes and vascular endothelial cells (See Practical Applications in Such as physiological events represent the rationale of biophysical-semeiotic bedside evaluation of leptin concentrations, augmented in metabolic syndrome and often in advanced stages of pre-metabolic syndrome, classic and variant. Thus, the possibility of recognizing, for the first time clinically, leptin increase constitutes a diagnostic tool of essential importance, applicable on very large scale.Recent studies with obese and non-obese humans demonstrated a strong positive correlation of serum leptin concentrations with percentage of body fat, and... read full comment

Comment on: Al-Daghri et al. Cardiovascular Diabetology, 6:18

Hypertensive Constitution accounts for the exsistence of diabetics with and without Hypertension. (Sergio Stagnaro, 21 October 2006)

Sirs.Interestingly,“clinical” biophysical semeiotic evidence demonstrates that natriuretic peptides (NP) act acutely to reduce plasma volume by at least 3 mechanisms: increased renal excretion of salt and water, vasodilation, and increased vascular permeability (1, 2, 3, 4). Fortunately, all these actions can nowadays be evaluated quantitatively, for the first time, at the bed-side by means of Biophysical-Semeiotics (See, Practical Applications) (2). Firstly, we can assess the basal vasodilation of whatever artery, e.g., of brachial artery, and, secondly, the NP-dependent artery dilation, according to methods described also in above-cited site (2, 3). At this point, from both diagnostic and prognostic view-point, it is really usefull the... read full comment

Comment on: Felício et al. Cardiovascular Diabetology, 5:19

"Bedside assessing ANS, RAAS, and IIR: a complex relation to type 2 diabetes". (Sergio Stagnaro, 15 November 2005)

I can't agree with the paper's conclusions "In frequency domain, the analysis of sympathetic (LF) and parasympathetic (HF) component evidenced an association between the offspring of type 2 diabetic subjects and a sympathetic overactivity. A global reduction and alteration of circadian rhythm of autonomic activity are present in offspring of type 2 diabetic patients with and without insulin resistance. The data of our study suggested that an autonomic impairment is associated with the familiarity for type 2 diabetes independently to insulin resistance and that an impairment of autonomic system activity could precede the insulin resistance..." In my opinion, such statements are not completely true as well as misleading, as allows me to state a 48-year-long clinical experience . Firstly... read full comment

Comment on: Fiorentini et al. Cardiovascular Diabetology, 4:15

Biophysical-Semeiotic Bed-Side Evaluating PPARs Activity in Metabolic Syndrome. (Sergio Stagnaro, 19 September 2005)

Sirs, in my 48-year-long clinical experience, the primary prevention of all components of metabolic syndrome, as IIR, IGT and type 2 diabetes, dyslipidaemia, is principally based on recognizing on very large scale Pre-Metabolic syndrome, classic and “variant” (See web site, Pre-Metabolic Syndrome, URL, and its early evolution to metabolic syndrome, since the well-known diabetes and dyslipidaemia complications begin years or decades before disorder onset. Dyslipidaemia is a major risk factor for atherosclerotic coronary heart disease, which in turn is the commonest cause of mortality in type 2 diabetes, caused by dyslipidaemia-dependent insulin-... read full comment

Comment on: Tenenbaum et al. Cardiovascular Diabetology, 4:14

Newer antioxidants should include the old antioxidant: sodium thiosulfate (Melvin Hayden, 27 June 2005)

First, congratulations on an excellent article in this exciting area of research. Sodium thiosulfate is emerging as a treatment for calciphylaxis. It is capable of donating its two unpaired electrons, is a scavenger of reactive oxygen - nitrogen species, and may generate glutathione. Additionally, it is an excellent chelator of calcium, which is a problem in diabetes resulting in medial vascular ossification – calcification.The peripheral arteriolopathy associated with diabetes and skin ulcerations are all too frequently recalcitrant to standard therapy and result in untold complications with eventual limb loss. It is entirely possible that therapy with sodium thiosulfate could promote healing of these ulcers and prevent limb loss by accelerating healing of these peripheral... read full comment

Comment on: Johansen et al. Cardiovascular Diabetology, 4:5

Important error in manuscript regarding low HDL-C (Melvin Hayden, 10 January 2005)

The chemistry profile of 2004 is in error.The uric acid level is reported to be 6.5 mg/dL with global risk reduction and this is in error.The correct uric acid level following global risk reduction is 3.5 mg/dL in 2004Elevations of uric acid levels greater than 4 mg/dL are to be considered a red flag and more agressive therapy should be initiated.Hayden MR, Tyagi SC: Uric acid: A new look at an old risk marker for cardiovascular disease, metabolic syndrome, and type 2 diabetes mellitus: The urate redox shuttle.Nutr Metab (Lond). 2004 Oct 19;1(1):10 read full comment

Comment on: Hayden et al. Cardiovascular Diabetology, 4:1

Homocysteine as a competitive inhibitor of ciprofibrate for PPAR alpha and gamma (Melvin Hayden, 29 July 2004)

Congratulations on an excellent study and publication. I really enjoyed this well written paper and viewing the results of this study. Homocysteine has been found to be a competitive inhibitor of PPAR alpha and gamma recently in our laboratory and may be playing an important role in your observations especially in those with BMI greater than 25 as compared to those with a BMI less than 25. I would suggest that the data might be changed by the addition of folic acid in these patients to lower the homocysteine and reexamine the results if possible.It would be exciting if you could examine the levels of homocysteine and see if there is any correlation to your exciting published results.Sincerely,M.R. Hayden, M.D.mrh29@usmo.comSee paper and references: Homocysteine and reactive oxygen... read full comment

Comment on: Aguilar-Salinas et al. Cardiovascular Diabetology, 3:8