We read with great interest the very important article by Dilaveris
et al about the climate impacts on myocardial infarction deaths in Athens,
Greece [1].
Several reports have already proved that the number of deaths related to
acute myocardial infarction (AMI) shows a seasonal variation, with a peak
in winter, and a lowest number of mortality rates during the months of
summer [2,3,4]. The effects o...
We read with great interest the very important article by Dilaveris
et al about the climate impacts on myocardial infarction deaths in Athens,
Greece [1].
Several reports have already proved that the number of deaths related to
acute myocardial infarction (AMI) shows a seasonal variation, with a peak
in winter, and a lowest number of mortality rates during the months of
summer [2,3,4]. The effects of meteorological variables on the human
organism have been studied for more than fifty years, and changes in the
number of AMI events have been related to both cold or warm temperatures
[5,6,7]. Some authors have found that the incidence of a hear attack may
also be influenced by changes of atmospheric pressure and front movements
[8,9].
Hungary is a small country in the middle of Europe, laying in the
Carpathian basin. Based on our results it may be stated that the number of
cardiac mortality (N=16.160) in Hungary shows a steadily decreasing
tendency between 2000 and 2005, with a seasonal variation regardless of
age or sex. Studying year 2001 in more detail, the peak period of AMI
mortality was during the months of spring, with a lowest value during the
summer. There was a significant difference between seasons (F=3.027;
p<0.05; N=2850). The daily average of cardiovascular mortality during
each season was the following: 8.48 during spring, 7.23 during the summer,
7.79 during autumn, and 7.76 during winter. The low rate of AMI mortality
during the months of summer may be related to summer holidays in addition
to favourable meteorological conditions. In addition to these findings, it
seems that the changes of weather conditions also influence the mortality
of other cardiovascular events. In Hungary the highest average daily
temperature in year 2001 was 28.83 Celsius grade in the month of July,
while the lowest average daily temperature was -10.93 Celsius grade in
December.
With consideration to meteorological conditions, our results show, that
the sharp temperature increase during spring, and the similarly
significant decrease of temperatures during autumn, both have an
increasing effect on heart attack related mortality. Studying the moving-
average of AMI mortality (k=7), and the relation with the daily average
temperature of the preceding 7 days, we have found a medium value negative
correlation (r = -0.466, p<0.01).
Categorizing our data according to age groups, the strongest correlation
was found in the age group of above 70 (r = -0.41, p<0.01), with a
weaker relation in the age group between 50 and 70 (r = -0.315,
p<0.01), while in the age group below 50 years of age, no correlation
was found. Considering the moving average of deaths (k=7) and the average
daily temperature of the preceding seven days above and below 20 Celsius
grade, we have found a significant difference. When the average daily
temperature of the preceding 7 days was above 20 Celsius grade, the
average of daily mortality was 7.23, while below 20 Celsius grade the
average of deaths was 7.93.
In the year 2001 in Hungary, the average daily atmospheric pressure showed
its lowest seasonal average during spring (with a value of 1013.14 hPa),
and the highest during autumn (1022.30 hPa). The moving average of deaths
during spring (k=7) shows a weak negative correlation with average daily
atmospheric pressure (r = -0.343, p<0.01).
This finding suggests, that the mortality of acute myocardial infarction
may be related to the internal biological rhythm of the organism, and also
to such external conditions as weather. From a biometeorological point of
view, the combined effect of certain meteorological factors, such as a
sudden temperature or atmospheric pressure change, or the number of front
movements, may be considered as a risk factor in the mortality of a heart
attack. The more risk factors one bares, the higher the chance of
developing a cardiovascular disease.
References
1. Dilaveris P, Synetos A, Giannopoulos G. et al. Climate Impacts on
Myocardial infarction deaths in the Athens Territory: the CLIMATE study. Heart 2006;92:1747-51.
2. Gerber Y, Jacobsen SJ, Killian JM. et al. Seasonality and daily weather
conditions in relation to myocardial infarction and sudden cardiac death
in Olmsted County, Minnesota, 1979 to 2002. J Am Coll Cardiol 2006;48:287-
92.
3. Sayer JW, Wilkinson P, Ranjadayalan K, et al. Attenuation or absence of
circadian and seasonal rhythms of acute myocardial infarction. Heart
1997;77:325-9.
4. Spencer FA, Goldberg RJ, Becker RC. et al. Seasonal distribution of
acute myocardial infarction in the second National Registry of Myocardial
Infarction. J Am Coll Cardiol 1998;3:1226-33.
5. Mestan JF, Kral V, Horni J. Meteorological effects on myocardial
infarct. Cas Lek Cesk 1956;95:581-5.
6. Ku CS, Yang CY, Lee WJ. et al. Absence of a seasonal variation in
myocardial infarction onset in a region without temperature extremes. Cardiology 1998;89:277-82.
7. Panagiotakos DB, Chrysohoou C, Pitsavos C. et al. Climatological
variations in daily hospital admissions for acute coronary syndromes. Int
J Cardiol 2004;94:229-33.
8. Houck PD, Lethen JE, Riggs MW. et al. Relation of atmospheric pressure
changes and the occurrences of acute myocardial infarction and stroke. Am
J Cardiol 2005;96:45-51.
9. Kveton V. Weather fronts and acute myocardial infarction. Int J
Biometeorol 1991;35:10-7.
We read with great interest the study by Wolferen et al1, which confirmed that addition of sildenafil reversed right ventricular (RV) dilatation and hypertrophy in pulmonary arterial hypertension (PAH) patients already receiving treatment and that these positive effects on RV structure and function occurred in parallel with improvements in exercise capacity and N-terminal pro-brain natriuretic peptide (NT-...
We read with great interest the study by Wolferen et al1, which confirmed that addition of sildenafil reversed right ventricular (RV) dilatation and hypertrophy in pulmonary arterial hypertension (PAH) patients already receiving treatment and that these positive effects on RV structure and function occurred in parallel with improvements in exercise capacity and N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations. The methods and interpretation of the results, however, raise several concerns:
In this study, the left ventricular diastolic function parameters, for example, E, A, and E-wave deceleration time, E/A ratio, the maximal velocity during early diastole, the maximal velocity during atrial contraction and the ratio of them of mitral annulus etc., however, were not included in baseline parameters. It is well known that the marked diastolic dysfunction which could be promoted by PAH inducing increased RV pressure typically displace the pressure-volume relationship in an upward direction, resulting in increased left ventricular end-diastolic, left atrial, and rising pulmonary capillary wedge pressures, even aggravating right ventricular dysfunction. And then, is there a significant difference of left ventricular diastolic function condition at baseline, 12 months bosentan and 12 months bosentan + 3 months combination of the study groups? Is there a relation of left ventricular diastolic function condition to therapeutic advantages offered by bosentan and combination therapy? Similarly, the difference of RV diastolic function at baseline, 12 months bosentan and 12 months bosentan + 3 months combination are not described. Is there a relation of the difference of RV diastolic function at baseline, 12 months bosentan and 12 months bosentan + 3 months combination to therapeutic advantages offered by bosentan and combination therapy? They needs to be further evaluated.
An echocardiography study of Lopez-Candales et al2 certify that a very strong correlation between RV mechanical delay and RV fractional area change was noted in patients with PAH, suggesting RV mechanical delay could be a mechanism of RV dysfunction induced by PAH. In this study, however, RV mechanical delay at baseline, 12 months bosentan and 12 months bosentan + 3 months combination were not described. It is very important because several new and effective treatment options for RV dysfunction induced by PAH which could significantly improve the prognosis of the PAH patients would be proposed, if there was a relation of the therapeutic advantages offered by bosentan and combination therapy to improvement of RV mechanical delay. Therefore, the mechanism of RV dysfunction induced by PAH and the therapeutic advantages offered by bosentan and combination therapy needs to be further evaluated.
References
1. Wolferen SAV, Boonstra A, Marcus JT, et al. Right ventricular reverse remodelling after sildenafil in pulmonary arterial hypertension. Heart 2006; 92: 1860-1861.
2. Lopez-Candales A, Dohi K, Bazaz R, et al. Relation of right ventricular free wall mechanical delay to right ventricular dysfunction as determined by tissue Doppler imaging. Am J Cardiol 2005; 96: 602-606.
I read with great interest the recent report from Schmid and
coworkers regarding the hemodynamic changes induced in water, which is of
special interest among patients with deteriorated cardiac function. The
hypothesis is interesting, however the methods used for cardiac output
determination in a swimming pool have to be discussed. Schmid used an
inert gas rebreathing method using an infrared photoa...
I read with great interest the recent report from Schmid and
coworkers regarding the hemodynamic changes induced in water, which is of
special interest among patients with deteriorated cardiac function. The
hypothesis is interesting, however the methods used for cardiac output
determination in a swimming pool have to be discussed. Schmid used an
inert gas rebreathing method using an infrared photoacustic gas analyser,
which has been validated in land situations only by the references given
by the authors. Gabrielsen (1) and coworkers studied 11 patients with
dilated cardiomyopathy or primary pulmonary hypertension regarding the
rebreathing technique vs. direct Fick measurement using a catheter in the
cath lab up to cardiac outputs of from 2 to 6.5l/min only. Agostoni (2)
and coworkers studied 20 patients with chronic heart failure (Vo2
16.6±2.9ml/min/kg) on a cycle ergometer vs. thermodilution and vs. Fick
method with good correlation from cardiac output of 4.5l/min to 12l/min.
As stated by the authors repetitive calibration is mandatory even in the
lab setting and we do not have any data from the authors regarding the
intra- and interobserver reliability of the rebreathing method used in the
swimming pool.
Schmid reported significant stroke volume changes from 60ml to more
than 100ml among healthy subjects with consecutive increase of cardiac
index from 2.3l/min/m2 to 5l/min/m2 in the healthy subjects. Systemic
vascular resistance decreased significantly in immersion using the
rebreathing method.
We tested thirteen cardiac healthy swimming athletes with real-time
continuous wave (CW) Doppler based hemodynamic monitoring using the USCOM
device (3) at rest at land, at immersion and following a swimming
endurance protocol. In contrast to rest at land whole body immersion
increased heart rate from 94±17/min to 100±14/min, stroke volume from
42±18ml to 81±18/ml, and cardiac output from 4.0±0.9l/min to 8±1.6l/min
(cardiac index 2.17±0.6l/min/m2 vs. 4.3±0.9l/min/m2), which is somehow in
line with the data presented by Schmid using the rebreathing method.
Systemic vascular resistance declined from 2053±469 to 986±249dyne*s*cm-5
significantly in our small study which also is in line with the reported
data from Schmid. The endurance swimming test lead to significant
upregulation of heart rate from baseline to 160±12/min, stroke volume
(95±9ml), cardiac output (15.4±1.6l/min), and cardiac index
(8.3±1.0l/min/m2).
Therefore, based on the results of Schmid using the rebreathing
method and our direct ultrasound cardiac monitoring using the USCOM in
healthy swimming athletes, significant changes of hemodynamics are
encountered in immersion at rest especially regarding the upregulation of
the stroke volume rather than an increased heart rate. Further studies are
mandatory to elucidate the immediate hemodynamic response among patients
with heart failure in physical exercise in the water, such as aqua
jogging, moderate swimming or even diving.
References
(1) Gabrielsen A, Videbaek R, Schou M, Damgaard M, Kastrup J, Norsk P. Non-invasive measurment of cardiac output in heart failure patients using a new foreign gas rebreathing technique. Clin Sci (Lond) 2002;102:247-52.
(2) Agostoni P, Cattadori G, Apostolo A, Contini M, Palermo P, Marenzi G, Wasserman K. Noninvasive measurment of cardiac output during exercise by inert gas rebreating technique: a new tool for heart failure evaluation. J Am Coll Cardiol 2005;46:1779-81.
(3) Knobloch K, Lichtenberg A, Winterhalter M, Rossner D, Pichlmaier M, Phillips R. Non-invasive cardiac output determination by twodimensional independent Doppler during and after cardiac surgery. Ann Thorac Surg 2005;80:1479-83.
We injoyed very much the most interesting study by Teo et al (1). Acute coronary syndromes(ACS) and coronary risk factors; hypertension, hyperlipidemia,obesity and type 2 diabetes have become a major health problem in Asia with economic development,due to interaction of gene and
environmental factors.(2) Overswinging,that is an excessive circadian variation in blood pressure (BP) has been associated with...
We injoyed very much the most interesting study by Teo et al (1). Acute coronary syndromes(ACS) and coronary risk factors; hypertension, hyperlipidemia,obesity and type 2 diabetes have become a major health problem in Asia with economic development,due to interaction of gene and
environmental factors.(2) Overswinging,that is an excessive circadian variation in blood pressure (BP) has been associated with a large increase in cardiovascular risk,present even in absence of hypertension and
prehypertension itself.The prevalence of obesity varies between 5-7%, in the Asian urban population.The paradox is that despite low rates of obesity, the prevalence of central obesity (40-60%),prediabetes(10-15%),overswinging of BP(10-15%),type 2 diabetes(6-15%),and ACS(9-14%) are
higher, in urban areas, which are much higher among Asian immigrants to developed countries(2).The prevalence of metabolic syndrome is 5% in rural and 15%in urban south India whereas in north and western India,the prevalences appear to be slightly lower. In a cross-sectional survey, in five Indian cities,among 6940 subjects aged 25years and above, the prevalence of obesity was approximately 7% but more than half of the subjects had central obesity and one third had prehypertension,one quarter hypertension and one fifth prediabetes.About three quarters of hypertensives had central obesity in both sexes. In a subsample,(n=1633), the prevalence of metabolic syndrome comprising of central obesity, hypertension and hypertriglyceridemia and low HDL was approximately 13% and premetabolic syndrome comprising of prehypertension, prediabetes and
central obesity in 19.5%. The emerging typical South Asian, urban or immigrant has phenotype of higher percentage of body fat at a lower value of BMI,high WHR at a relatively low waist circumference and less lean body
mass compared to other ethnic groups. A similar genotype is present among Chinese and other Asians.However,in case control studies,the mean age in south Asia varies between 48 to 51 years,which is againt the finding of 61 years mean age among Asians,(3) in the study by Teo and co-workers(1,3).
In one study among 54 patients with acute coronary syndromes(ACS), 41 patients had acute myocardial infarction(AMI),5 possible MI, 4 cases unstable angina and rest 4 angina pectoris.The control subjects(n=85) were randomly selected from the population from the city of Moradabad, drawn from a similar age and sex of the subjects.Serum level of nitrite(a indicator of nitric oxide,NO) was significantly lower in patients with AMI compared to controls(mean+SD:0.36+1.42 vs 0.96+1.48uM,CI difference
0.60,0.34-1.02,P<0.03).After 4 weeks of follow up,serum nitrite level recovered showing significant increase without such changes in the control group.(0.88 vs 1.09uM;CI 0.21,0.67-1.12,P<0.05) The incidence of
lipoprotein(a) excess(>30mg/dl) and mean levels of
lipoprotein(a)(difference 6.4mg/dl,95% confidence interval 2.8-10.5,P<0.05) was significantly greater in the acute CAD group compared to control subjects.Serum levels of vitamins E,C and beta-carotine,coenzyme Q10,magnesium and potassium were significantly lower and insulin, glucose, triglycerides, and lipoprotein(a) were significantly higher
in ACS compared to their levels after 4 weeks of follow up.There was a significantly greater occurrence of acute ACS events in the second quarter of the day compared to other quarters.A circadian rhythm was also noted
for serum level of NO showing significantly lower nitrite in 6.00-12.00 AM period compared to afternoon,12.00-18.00hours period(0.27+1.12 vs 0.42+1.44 uM,P<0.04).
The differences in the nitrite levels in the two groups indicate that low levels of nitrite appears to be a risk factor of ACS.Lower levels of nitrite during acute stage of AMI and its recovery after 4 weeks of follow up indicate that transient hyperglycemia and hyperinsulinemia may also be responsible for its increase, (apart from low arginine intake and sedentary behaviour,) by inhibiting the expression of NO receptors caused by metabolic reactions evoked by ACS. Reduction in antioxidants vitamins may be due to increased oxidative stress which is common in AMI due to enhanced free radical generation which may also influence NO levels and cause endothelial dysfunction.More studies would be necessary to
demonstrate that NO deficiency is a risk factor of ACS.There is a need to compare association of protective factors; physical activity, fruit and begetable intake,n-6/n-3 ratio in the diet, moderate alcohol intakes and
stress to find out their roles in the pathogenesis of ACS among Asians and Caucasians(1-5).
In rural population of India and China,there is low plasma insulin, low glucose, triglycerides and angiotensin. There is low prevalence of central obesity and obesity is uncommon in rural areas of Asia.When these
populations migrate to urban slums or to industrialized countries, they substitute cereal based diet from ready prepared fast foods containing more linoleic acid, saturated fat, trans fatty acids, sugar, and flesh
foods and dairy products in conjunction with sedentary behaviour and increased mental stress.It seems that rapid changes in diet and lifestyle due to modest but unsustainable, economic development, without learning of
methods of prevention, result into maladaptations, that are important in the pathogenesis of acute coronary syndromes among Asians.
icn2008@mickyonline.com
REFERENCES
1.Teo M, Lalondrel S, Roughton M, Mason RG, Dubrey SW Acute coronary syndromes and their presentation in Asian and Caucasian patients in Britain Heart 2007, 93: 183-188
2.Singh RB, Suh IL, Singh VP et al. Hypertension and stroke in Asia;prevalence, control, and strategies in developing countries for prevention J Human Hyper 2000 ,14:740-763
3.Singh RB,Rastogi SS, Verma R et al. An Indian experiment with nutritional modulation in acute myocardial infarction Am J Cardiol 1992, 69: 879-885
4.Singh RB, Pella D, De Meester F What to eat and chew in acute myocardial infarction Eur Heart J 2006,27: 1628-29
5.Janus ED, Postiglion E, Singh RB, Lewis B. Coronary heart disease in Asia Circulation 1996,94: 2671-73
At the out-set, I want to congratulate the authors of the article "The patho-physiology of myocardial reperfusion: a pathologist's perspective" (1)for an outstanding job in summarizing a complex topic in a
simplified way.
However, it was presented as if “reperfusion” is the culprit ("Reperfusion Injury”), even though, an attempt is made to clarify that the injury after reperfusion is happenin...
At the out-set, I want to congratulate the authors of the article "The patho-physiology of myocardial reperfusion: a pathologist's perspective" (1)for an outstanding job in summarizing a complex topic in a
simplified way.
However, it was presented as if “reperfusion” is the culprit ("Reperfusion Injury”), even though, an attempt is made to clarify that the injury after reperfusion is happening from previous ischemia, from present reperfusion and from ischemia that is present in the micro-
vasculature despite reperfusion. There were multiple reference articles that were quoted which again use the term" reperfusion injury" (2-4) adding to the impression that reperfusion is the "only" culprit, which in-fact, is playing a “partial” role.
From the available experimental data, we totally agree that “reperfusion associated injury” is real and proven. As agreed by authors in their article, reperfusion is only a part of this problem (while, in fact, it is the solution to the problem of coronary ischemia). It helps to have a proper terminology for this complex phenomenon so that whole gamut of the problem is reflected in the terminology rather than a part. We strongly feel that a proper terminology makes a huge difference in proper understanding, especially when a complex phenomenon is involved.
“Myocardial ischemia and reperfusion injury” (5) may be one terminology close this phenomenon than “reperfusion injury”, as it implies that the injury is happening both from ischemia and reperfusion rather than reperfusion alone.
A most appropriate terminology, we feel, is “Reperfusion Micro-vascular Ischemia (RMI)”(6) as coined by Spears et al , which signifies that the injury is caused by ischemia, reperfusion and persistent micro-vascular dysfunction despite reperfusion, rather than “reperfusion injury” alone.
References:
1. Basso C, Thiene G The pathophysiology of myocardial reperfusion: a pathologist's perspective Heart (British Cardiac Society). Nov 2006;92(11):1559-1562
2. Ambrosio G, Tritto I Reperfusion injury: experimental evidence and clinical implications American heart journal. Aug 1999;138(2 Pt 2):S69-75
3. Kloner RA Does reperfusion injury exist in humans? Journal of the American College of Cardiology. Feb 1993;21(2):537-545
4. Maxwell SR, Lip GY Reperfusion injury: a review of the pathophysiology, clinical manifestations and therapeutic options International journal of cardiology. Jan 31 1997;58(2):95-117
6. Spears JR, Prcevski P, Xu R, Li L, Brereton G, DiCarli M, Spanta A, Crilly R, Lavine S, vander Heide R Aqueous oxygen attenuation of reperfusion microvascular ischemia in a canine model of myocardial infarction Asaio J. Nov-Dec 2003;49(6):716-720
With interest we read the article by McMahon et al. about the application of tissue Doppler imaging (TDI) in assessing the prognosis of children with left ventricular hypertrabeculation/noncompaction (LVHT).[1]
We have, however, several questions and concerns:
There are only limited experiences in the follow-up of patients with LVHT and the prognosis is largely unknown.[2] The “undul...
With interest we read the article by McMahon et al. about the application of tissue Doppler imaging (TDI) in assessing the prognosis of children with left ventricular hypertrabeculation/noncompaction (LVHT).[1]
We have, however, several questions and concerns:
There are only limited experiences in the follow-up of patients with LVHT and the prognosis is largely unknown.[2] The “undulating phenotype” of the cardiac abnormalities is a feature of LVHT, not exclusively found in children, but also in adults.[3]
With interest we recognized that the applied diagnostic criteria are a fruitful combination of Jenni’s and our criteria. Recently we proposed to classify LVHT cases fulfilling both criteria as “definite” and fulfilling
either criterion as “probable” LVHT.[4] How was “dilated”, “hypertrophic” and “combined” phenotype defined?
It is well known that TDI parameters and measurements are influenced by the type of the echocardiographic machine.[5] Did the authors observe different results when using different machines? Were interobserver variability studies performed regarding registration of the TDI signals?
Were there any correlations between heart rate or blood pressure and the parameters measured by TDI?
We miss information about the gender of the included patients, and results of the 2-D and M-mode echocardiographic measurements, like left ventricular wall thickness or enddiastolic diameter. Why were these
parameters not included in the calculation of the Cox model? It cannot be excluded that conventional 2-D and M-mode echocardiographic parameters are predictors for prognosis of equal emphasis as TDI parameters.
According to which protocol were the follow-up investigations performed?
How to explain the discrepancy of patient recruitment starting in January 1999 and the maximal follow-up duration of 132 months? How many thromboembolic events occurred during follow-up?
How to explain the threefold increased mortality in the presented cohort compared to the 5.3% mortality/year as observed in adults?[2]
In the two patients with dysmorphic features, which genetic syndrome was diagnosed? Did these two patients also present with skeletal muscle abnormalities? At least in adults, LVHT is frequently associated with neuromuscular disorders. How many of the included 56 patients were seen by a neurologist, and in how many was a neurological disorder detected?
Interestingly, in 4 patients LVHT affected the interventricular septum.
Septal LVHT is extremely rare, thus it would be of interest to have more information about these patients.
If the authors assume that TDI is influenced by LVHT, why did they choose movement of the basal parts of the ventricle for registration, where no LVHT is located, and not the midventricular or apical parts of the left
ventricle, where LVHT is usually located? Which explanation do the authors have for their observation of decreased velocities as assessed by TDI in LVHT? Did the velocities change in patients with undulating phenotype in
accordance with improvements in left ventricular systolic function?
In conclusion, before assessing TDI parameters as useful parameters to predict outcome of patients with LVHT, information about other echocardiographic findings and extracardiac comorbidities is necessary.
References
1. McMahon CJ, Pignatelli RH, Nagueh SF, Lee VV, Vaughn W, Valdes SO, Kovalchin JP, Jefferies JL, Dreyer WJ, Denfield SW, Clunie S, Towbin JA, Eidem BW Left ventricular noncompaction cardiomyopathy in children: Characterization of clinical status using tissue Doppler-derived indices of left ventricular diastolic relaxation Heart 2006 Nov 29;ePub
2. Stöllberger C, Winkler-Dworak M, Blazek G, Finsterer J Prognosis of left ventricular hypertrabeculation/noncompaction is dependent on cardiac
and neuromuscular comorbidity Int J Cardiol 2006; in press
3. Stöllberger C, Keller H, Finsterer J Disappearance of left ventricular hypertrabeculation/noncompaction after biventricular pacing in a patient with myopathy J Card Fail 2006; in press
4. Finsterer J, Stöllberger C Definite, probable , and possible left ventricular hypertrabeculation/noncompcation Int J Cardiol 2006; in press
5. Kjaergaard J, Korinek J, Belohlavek M, Oh JK, Sogaards Hassager C Accuracy, reproducibility, and comparability of Doppler tissue imaging by two high-end ultrasound systems J Am Soc Echocardiogr 2006;19:322-8
Dr. Huffman and colleagues [1] studied 131 post-myocardial infarction
(MI) patients (17 with major depressive disorder [MDD]) and reported that
two items from the Beck Depression Inventory (BDI) related to sadness and
loss of interest formed an effective screening tool for post-MI
depression. The sensitivity and specificity results reported by Huffman et
al. are, in fact, highly similar to those repo...
Dr. Huffman and colleagues [1] studied 131 post-myocardial infarction
(MI) patients (17 with major depressive disorder [MDD]) and reported that
two items from the Beck Depression Inventory (BDI) related to sadness and
loss of interest formed an effective screening tool for post-MI
depression. The sensitivity and specificity results reported by Huffman et
al. are, in fact, highly similar to those reported for two other existing
brief depression screens, the PHQ-2 [2], which was validated in a sample
of 580 primary care patients (41 with MDD), and a similar 2-item screen
[3], which was validated in a sample of 1,024 patients with coronary heart
disease (CHD) (224 with MDD). The validation study for the CHD screen
included a comparison to the PHQ-2 and found identical areas under the
curve (a measure of overall accuracy) of 0.84 for both instruments and
sensitivities and specificities that were very similar to those reported
by Huffman et al.when a cutoff of 1 or greater was used for each
instrument. Notably, these two screening tools and the screening tool
proposed by Huffman et al. each include slightly differently worded
versions of 2 items: an item about mood and an item about anhedonia, the
two core symptoms of a DSM-IV diagnosis of MDD.
Is it beneficial to continue to look for “new” and slightly different
versions of brief depression screening tools? The authors of a literature
synthesis of case-finding instruments for identifying depression in
primary care concluded that it is not [4]. They found 16 case-finding
instruments of 1-30 items that all had adequate performance
characteristics in primary care and found very few differences between
instruments (although there were significant differences within
instruments across studies) . In their words, “the search for a better
mousetrap has not led to an instrument with superior performance
characteristics.” Furthermore, the proliferation of new instruments with
no notable improvement in performance has the potential to create
confusion, but not better options, for clinicians and researchers.
While the search for “a better mousetrap” is not likely to add much
to the clinical care of MI patients, a simple mousetrap is clearly
desirable for use in acute cardiac care, since MI patients are generally
cared for by cardiovascular specialists whose focus is not on depression
and who often do not have the expertise to diagnose or treat this
condition. However, the question is not whether a few simple questions
can improve rates of recognition of depression in busy cardiac units.
Rather, it is whether cardiovascular specialists can and will use these
screening tools, and how they would perform in their hands under real life
conditions rather than when administered by psychiatrists as in the study
by Huffman, et al.1 In addition, research is needed that attends to
essential, but generally neglected, elements of the screening process,
such as when, where, and how often to screen patients; whether patient
characteristics, such as age, gender, and race, influence the accuracy of
depression screening in the post-MI setting; and, as noted by the authors,
whether serial screening with more than one instrument improves efficiency
and accuracy.
REFERENCES
1. Huffman JC, Smith FA, Blais MA, Beiser ME, Januzzi JL, Fricchione GL. Rapid screening for major depression in post-myocardial infarction patients: an investigation using Beck Depression Inventory II items. Heart 2006;92:1656-60.
2. Kroenke K, Spitzer RL, Williams JB. The Patient Health Questionnaire-2: validity of a two-item depression screener. Med Care 2003;41:1284-92.
3. McManus D, Pipkin SS, Whooley MA. Screening for depression in patients with coronary heart disease (data from the Heart and Soul Study). Am J Cardiol 2005;96:1076-81.
4. Williams JW,Jr, Pignone M, Ramirez G, Perez Stellato C. Identifying depression in primary care: a literature synthesis of case-finding instruments. Gen Hosp Psychiatry 2002;24:225-37.
The Committee for the Safety of Medicines has only two entries for amiodarone extravasation injury, yet almost every consultant seems to remember a patient who has had their arm amputated following extravasation of amiodarone. Surely this is a case of the dangers of peripheral
amiodarone being exagerated? In periarrest / cardiac arrest situations amiodarone has been given as a peripheral bolus countl...
The Committee for the Safety of Medicines has only two entries for amiodarone extravasation injury, yet almost every consultant seems to remember a patient who has had their arm amputated following extravasation of amiodarone. Surely this is a case of the dangers of peripheral
amiodarone being exagerated? In periarrest / cardiac arrest situations amiodarone has been given as a peripheral bolus countless times; what proportion of cases result in extravasation injury?
Central line access has many potential complications /
contraindications (e.g. post thrombolysis). If the patient is on ITU and has a central line - great - otherwise the delay and risk involved in inexperienced juniors obtaining central access appear to me to outweigh the tiny risk of extravasation injury; providing the amiodarone is given
through a fresh antecubital fossa venflon.
This Heart article has also been featured in the BMJ and it appears to be a case of a blanket guideline being made on anecdotal evidence.
Skin necrosis is a recognised complication of amiodarone infusion, but how does it compare with the risks of central venous cannnulation? The risks are considerable (and potentially fatal), especially if performed by
inexperienced junior staff, or in units with no Sonosite or other ultrasound device.
I think, for many patients, it is reasonable to deliver amiodarone via a large perip...
Skin necrosis is a recognised complication of amiodarone infusion, but how does it compare with the risks of central venous cannnulation? The risks are considerable (and potentially fatal), especially if performed by
inexperienced junior staff, or in units with no Sonosite or other ultrasound device.
I think, for many patients, it is reasonable to deliver amiodarone via a large peripheral vein.
From April 2002 until now, our hospital performed 1006 percutaneous coronary interventions (PCIs) without surgical backup on-site. Our total case load is now about 1500 coronary angiograms and 375 PCIs per year, and the number of PCIs performed has increased steadily during the period 2002-2006. In order to improve the access to PCI, a firm debate is ongoing in Belgium whether to choose for stand alone...
From April 2002 until now, our hospital performed 1006 percutaneous coronary interventions (PCIs) without surgical backup on-site. Our total case load is now about 1500 coronary angiograms and 375 PCIs per year, and the number of PCIs performed has increased steadily during the period 2002-2006. In order to improve the access to PCI, a firm debate is ongoing in Belgium whether to choose for stand alone PCI centres or to create more surgery programs for the sole purpose of supporting PCI. The article of J.
Carlsson et al. (1) from Sweden in this journal supports the first option.
The publication of K. Burton et al. (2) in this journal, which showed that there is no difference in death and myocardial infarction between low and high volume PCI centres in Scotland, is also very interesting in this respect.
However we would like to get some more information on this subject.
On the basis of these data we cannot deduce how safe it was to perform PCI in hospitals without on-site cardiac surgery. In the discussion of the article on page 1671 is mentioned: “Low-volume hospitals are less likely to have on-site surgical facilities.” However no information about this item is given in the methods or/and the results.
All of the 17 417 procedures were performed in six hospitals during 36 hospital years. If possible, we would like to know how many of these six hospitals had cardiac surgery on-site. Further more we can imagine that the use of surgery on-site will have changed over the years; this is why we want to know how many procedures were performed without surgical backup on-site. Finally was there a difference in major complications between hospitals with and without surgical backup on-site?
These data can be of great interest for the ongoing debate whether or not on-site cardiac surgical backup is still necessary for PCI. From a health care point of view, access to the best therapy for the greatest numbers of patients is an important goal. There is no doubt that, on the field, PCI has proven to be the best therapy in ST-elevation myocardial infarction (3, 4). Legitimating of hospitals to perform PCIs without cardiac surgery on-site, will improve access and could thereby lower mortality. Recommendations on this topic are given in literature by
experts working in Europe as well in North America (5, 6). It is in the best interest of our patients and the society, to stop the discussion between the haves and the have nots and to stop recommending against PCI in hospitals without surgical backup on-site.
References
1. Carlsson J, James SN, Stahle E, et al. Outcome of percutaneous coronary intervention in hospitals with and without on-site cardiac surgery standby. Heart published online first 15 September 2006.
2. Burton KR, Slack R, Oldroyd KG, et al. Hospital volume of throughput and periprocedural and medium-term adverse events after percutaneous coronary intervention: retrospective cohort study of all 17 417 procedures undertaken in Scotland, 1997-2003. Heart 2006; 92: 1667-1672.
3. Stenestrand U, Lindbäck J, Wallentin L. Long-term outcome of primary percutaneous coronary intervention vs. prehospital and in-hospital thrombolysis for patients with ST-elevation myocardial infarction. JAMA 2006; 296: 1749-1756.
4. Clemmensen P, Jurlander B. Primary PCI for ST elevation AMI saves lives and money-what more do we want? Editorial. Scand Cardiovasc J 2005; 39: 264-266.
5. Montalescot G, Anderson HR, Antoniucci D, et al. Summary of recommendations on percutaneous coronary intervention for the reperfusion of acute ST elevation myocardial infarction. Heart 2004; 90: 676-677.
6. Ting HT, Raveendram G, Lennon RJ, et al. A total of 1,007 percutaneous coronary interventions without onsite cardiac surgery. Acute and long term outcomes. J Am Coll Cardiol 2006; 47: 1713-21.
Conflict of interest/financial disclosure: There are no conflicts of interest and no financial disclosures.
Antoon. E. Weyne M.D., F.A.C.C.(1), Johan F. Vandenbogaerde M.D.(1), Philippe G. Dejaegher M.D.(1), Robert Van den Oever M.D.(2)
(1) Department of Cardiology, AZ Groeninge, Kortrijk, Belgium
(2) Director Health Policy, LCM, Brussels
Dear Editor,
We read with great interest the very important article by Dilaveris et al about the climate impacts on myocardial infarction deaths in Athens, Greece [1]. Several reports have already proved that the number of deaths related to acute myocardial infarction (AMI) shows a seasonal variation, with a peak in winter, and a lowest number of mortality rates during the months of summer [2,3,4]. The effects o...
Dear Editor,
We read with great interest the study by Wolferen et al1, which confirmed that addition of sildenafil reversed right ventricular (RV) dilatation and hypertrophy in pulmonary arterial hypertension (PAH) patients already receiving treatment and that these positive effects on RV structure and function occurred in parallel with improvements in exercise capacity and N-terminal pro-brain natriuretic peptide (NT-...
Dear Editor,
I read with great interest the recent report from Schmid and coworkers regarding the hemodynamic changes induced in water, which is of special interest among patients with deteriorated cardiac function. The hypothesis is interesting, however the methods used for cardiac output determination in a swimming pool have to be discussed. Schmid used an inert gas rebreathing method using an infrared photoa...
Dear Editor,
We injoyed very much the most interesting study by Teo et al (1). Acute coronary syndromes(ACS) and coronary risk factors; hypertension, hyperlipidemia,obesity and type 2 diabetes have become a major health problem in Asia with economic development,due to interaction of gene and environmental factors.(2) Overswinging,that is an excessive circadian variation in blood pressure (BP) has been associated with...
Dear Editor,
At the out-set, I want to congratulate the authors of the article "The patho-physiology of myocardial reperfusion: a pathologist's perspective" (1)for an outstanding job in summarizing a complex topic in a simplified way.
However, it was presented as if “reperfusion” is the culprit ("Reperfusion Injury”), even though, an attempt is made to clarify that the injury after reperfusion is happenin...
Dear Editor,
With interest we read the article by McMahon et al. about the application of tissue Doppler imaging (TDI) in assessing the prognosis of children with left ventricular hypertrabeculation/noncompaction (LVHT).[1]
We have, however, several questions and concerns:
There are only limited experiences in the follow-up of patients with LVHT and the prognosis is largely unknown.[2] The “undul...
Dear Editor,
Dr. Huffman and colleagues [1] studied 131 post-myocardial infarction (MI) patients (17 with major depressive disorder [MDD]) and reported that two items from the Beck Depression Inventory (BDI) related to sadness and loss of interest formed an effective screening tool for post-MI depression. The sensitivity and specificity results reported by Huffman et al. are, in fact, highly similar to those repo...
Dear Editor,
The Committee for the Safety of Medicines has only two entries for amiodarone extravasation injury, yet almost every consultant seems to remember a patient who has had their arm amputated following extravasation of amiodarone. Surely this is a case of the dangers of peripheral amiodarone being exagerated? In periarrest / cardiac arrest situations amiodarone has been given as a peripheral bolus countl...
Dear Editor,
Skin necrosis is a recognised complication of amiodarone infusion, but how does it compare with the risks of central venous cannnulation? The risks are considerable (and potentially fatal), especially if performed by inexperienced junior staff, or in units with no Sonosite or other ultrasound device.
I think, for many patients, it is reasonable to deliver amiodarone via a large perip...
Dear Editor,
From April 2002 until now, our hospital performed 1006 percutaneous coronary interventions (PCIs) without surgical backup on-site. Our total case load is now about 1500 coronary angiograms and 375 PCIs per year, and the number of PCIs performed has increased steadily during the period 2002-2006. In order to improve the access to PCI, a firm debate is ongoing in Belgium whether to choose for stand alone...
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